Evidence Report/Technology Assessment 

Number 156

Antiretroviral (ARV) Drug Resistance in the 

Developing World 

Prepared for: 

Agency for Healthcare Research and Quality 

U.S. Department of Health and Human Services 

540 Gaither Road 

Rockville, MD 20850 

www.ahrq.gov 

Contract No. 290-02-0003

Prepared by: 

Southern California Evidence-based Practice Center, Santa Monica, CA 

Authors 

Center Director 

Paul Shekelle, M.D., Ph.D. 

Associate Director 

Margaret Maglione, M.P.P. 

Content Experts 

Matthew Bidwell Goetz, M.D. 

Glenn Wagner, Ph.D. 

Graduate Student Assistant 

Zhen Wang, M.S. 

Programmer/Analyst 

Lara Hilton, B.A. 

Staff Assistants 

Jason Carter, B.A. 

Susan Chen, B.A. 

Carlo Tringale, BA 

Physician Reviewer 

Walter Mojica, M.D. 

Medical Editor 

Sydne Newberry, Ph.D. 

AHRQ Publication No. 07-E014 

September 2007 
 

This report is based on research conducted by the Southern California Evidence-based Practice 

Center (EPC) under contract to the Agency for Healthcare Research and Quality (AHRQ), 

Rockville, MD (Contract No. 290-02-0003). The findings and conclusions in this document are 

those of the author(s), who are responsible for its content, and do not necessarily represent the 

views of AHRQ. No statement in this report should be construed as an official position of AHRQ 

or of the U.S. Department of Health and Human Services. 

The information in this report is intended to help clinicians, employers, policymakers, and others 

make informed decisions about the provision of health care services. This report is intended as a 

reference and not as a substitute for clinical judgment. 

This report may be used, in whole or in part, as the basis for the development of clinical practice 

guidelines and other quality enhancement tools, or as a basis for reimbursement and coverage 

policies. AHRQ or U.S. Department of Health and Human Services endorsement of such derivative 

products may not be stated or implied. 
ii 

This document is in the public domain and may be used and reprinted without permission except 

those copyrighted materials noted for which further reproduction is prohibited without the 

specific permission of copyright holders. 

Suggested Citation: 

Maglione M, Geotz M, Wang Z, Wagner G, Hilton L, Carter J, Tringale C, Newberry S, Shekelle 

P. Antiretroviral (ARV) Drug Resistance in the Developing World. Evidence Report/ 

Technology Assessment No. 156. (Prepared by the Southern California Evidence-based Practice 

Center, under Contract No. 290-02-0003). AHRQ Publication No. 07-E014. Rockville, MD: 

Agency for Healthcare Research and Quality. September 2007.

Financial Disclosure Statement: No investigators have any affiliations or financial 

involvement (e.g., employment, consultancies, honoraria, stock ownership or options, 

expert testimony, grants or patents received or pending, or royalties) that conflict with 

material presented in the report.
iii 

Preface 

 The Agency for Healthcare Research and Quality (AHRQ), through its Evidence-Based 

Practice Centers (EPCs), sponsors the development of evidence reports and technology 

assessments to assist public- and private-sector organizations in their efforts to improve the 

quality of health care in the United States. This report was requested by the Fogarty International 

Center at the National Institutes of Health (NIH). The reports and assessments provide 

organizations with comprehensive, science-based information on common, costly medical 

conditions and new health care technologies. The EPCs systematically review the relevant 

scientific literature on topics assigned to them by AHRQ and conduct additional analyses when 

appropriate prior to developing their reports and assessments. 

 To bring the broadest range of experts into the development of evidence reports and health 

technology assessments, AHRQ encourages the EPCs to form partnerships and enter into 

collaborations with other medical and research organizations. The EPCs work with these partner 

organizations to ensure that the evidence reports and technology assessments they produce will 

become building blocks for health care quality improvement projects throughout the nation. The 

reports undergo peer review prior to their release. 

 AHRQ expects that the EPC evidence reports and technology assessments will inform 

individual health plans, providers, and purchasers, as well as the health care system as a whole, 

by providing important information to help improve health care quality. 

 We welcome comments on this evidence report. They may be sent to: Director, Center for 

Outcomes and Evidence, Agency for Healthcare Research and Quality, 540 Gaither Road, 

Rockville, MD 20850. 

Carolyn M. Clancy, M.D. 

Director 

Agency for Healthcare Research and Quality 

Roger I. Glass, M.D., Ph.D. 

Director 

Fogarty International Center 

Jean Slutsky, P.A., M.S.P.H. 

Director, Center for Outcomes and Evidence 

Agency for Healthcare Research and Quality 

Beth A. Collins Sharp, R.N., Ph.D. 

Director, EPC Program 

Agency for Healthcare Research and Quality 

Margaret Coopey, R.N., M.G.A., M.P.S. 

EPC Program Task Order Officer 

Agency for Healthcare Research and Quality 
iv 
v 

Structured Abstract 

Objectives: To describe the overall prevalence of ARV resistance in the developing world, 

focusing on: (1) treatment naïve populations, (2) the resistance consequences of prevention of 

mother to child transmission (pMTCT) drug regimens, and (3) the relationship of medication 

adherence to resistance. 

Data sources: We searched PubMed®, EMBASE, the Cochrane Controlled Clinical Trials 

Register Database, and the Cochrane Database of Reviews of Effectiveness (DARE). Additional 

sources of evidence included the Stanford University HIV Drug Resistance Database; reports of 

WATCH: Worldwide Analysis of Resistance Transmission over Time of Chronically and Acute 

Infected HIV-1 infected persons; a recent unpublished pMTCT overview; and various 

conference proceedings. Studies that did not report original research, that reported data already 

reported in another article, and case studies of fewer than 20 individuals were excluded. Of 1,122 

titles identified, 117 journal articles and presentations were included. 

Review methods: We abstracted data on geographic region, number of participants, subject 

demographics, HIV viral clade, medications taken (if any), years of data collection, how people 

were selected for resistance testing, and how and when resistance was assessed. Because of study 

heterogeneity, pooling was not possible; thus, the data are summarized qualitatively. Differences 

by region, population group, and HIV viral clade are described. 

Results: The patterns of ARV resistance among treatment naïve populations worldwide appear 

to reflect geographic trends in use of ARV medications. A worldwide surveillance program 

(WATCH) found the rate of resistance (to any drug) among treatment naïve individuals was 5.5 

percent in Africa, 7.4% in East Asia, 5.7 percent in Southeast Asia, and 6.4 percent in Latin 

America, lower than in North America (11.4 percent) and Europe (10.6 percent). 

Resistance data on HIV clades other than A, B, C, and D were too scarce to permit reliable 

conclusions. We also identified very few studies designed to assess the effect of health services 

delivery factors or medication adherence on the development of resistance in patients in 

developing countries. 

Evidence provided by longitudinal analyses suggests that, among women taking intrapartum 

single dose nevirapine (SD-NVP) to prevent mother-to-child transmission of HIV, both the 

overall prevalence of NNRTI resistance as well as the frequency of mutant virus in the overall 

viral population decreases with time since SD-NVP prophylaxis was received. 

Conclusions: In future resistance studies, rare HIV clades should be over-sampled in order to 

provide statistically meaningful data. Resistance surveillance programs should be maintained 

throughout the developing world, and data should be reported and analyzed in a consistent and 

timely manner. Where resources permit, studies of adherence in developing regions should 

conduct resistance testing. 
vi 
vii 

Contents 

Executive Summary......................................................................................................................1 

Evidence Report .........................................................................................................................9

Chapter 1. Introduction ...............................................................................................................11 

Frequency of ARV Resistance..............................................................................................12 

Determination of ARV Resistance........................................................................................12 

Chapter 2. Methods.....................................................................................................................15 

Original Proposed Key Questions.........................................................................................15 

Technical Expert Panel .........................................................................................................15 

Literature Search...................................................................................................................16 

Additional Sources of Evidence............................................................................................16 

Stanford University HIV Drug Resistance Database......................................................16 

WATCH: Worldwide Analysis of Resistance Transmission over Time of 

Chronically and Acute Infected HIV-1 Infected Persons ...............................................17 

Presentation – Preventing Mother-to-Child HIV Transmission and ARV 

Drug Resistance ..............................................................................................................17

Article – The Global Status of Resistance to ARV Drugs..............................................17 

Conference on Retroviruses and Opportunistic Infections (CROI)................................17 

International AIDS Conference ......................................................................................18 

IAS Conference on HIV Pathogenesis and Treatment ...................................................18 

Meetings of the Infectious Diseases Society of America ...............................................18 

Article Review ......................................................................................................................18 

Study Inclusion ...............................................................................................................18 

Screening.........................................................................................................................19 

Extraction of Study-Level Variables and Results.................................................................20 

Synthesis of Results ..............................................................................................................20 

Peer Review ..........................................................................................................................20 

Chapter 3. Results .......................................................................................................................21 

Description of the Studies.....................................................................................................21 

Published overviews .............................................................................................................23 

Treatment naïve persons in developing regions....................................................................24 

India ................................................................................................................................24 

Other Developing Nations in Asia..................................................................................27 

Latin America .................................................................................................................29 

Africa ..............................................................................................................................33 

Pregnant Women and Their Children, Developing Countries..............................................40 

Overview.........................................................................................................................40 

Resistance and pMTCT Regimen ...................................................................................40 

Adherence and health service issues.....................................................................................63 
viii 

Chapter 4. Discussion .................................................................................................................66 

Limitations ............................................................................................................................66 

Conclusions and Recommendations for Future Research ....................................................67 

References...................................................................................................................................69 

Tables 

Table 1. Treatment Naïve Data - India .......................................................................................26 

Table 2. Treatment Naïve Data - Asia ........................................................................................28 

Table 3. Treatment Naïve Data - Latin America ........................................................................31 

Table 4. Treatment Naïve Data - Africa .....................................................................................35 

Table 5. Studies of single-dose nevirapine .................................................................................41 

Table 6. Resistance after single-dose nevirapine, HIV clade C..................................................45 

Table 7. Resistance after single-dose nevirapine, other HIV clades...........................................46 

Table 8. Specific mutations observed in mothers receiving single-dose nevirapine ..................48 

Table 9. Resistance in women taking nevaripine to prevent mother-to-child transmission 

fades over time. ..........................................................................................................51 

Table 10. Other pMTCT regimens..............................................................................................54 

Table 11. Standard versus more sensitive tests...........................................................................57 

Table 12. Resistance in HIV positive infants born to mothers receiving pMTCT .....................61 

Figures 

Figure 1. Literature Flow ............................................................................................................22 

Appendixes 

Appendix A. Technical Expert Panel and Peer Reviewers 

Appendix B. Search Strings 

Appendix C. Data Collection Forms 

Appendix D. Evidence Tables 

Appendix E. Rejected Titles 

Appendixes and Evidence Tables for this report are provided electronically at 

http://www.ahrq.gov/downloads/pub/evidence/pdf/antiretro/antiret.pdf.
1 

Executive Summary 

Introduction 

The clinical management of HIV infection has greatly improved through the use of highly 

active antiretroviral therapy (HAART),1 which comprises the following classes of agents: 

nucleoside or nucleotide reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse 

transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and fusion inhibitors. The clinical 

effectiveness of these therapies is mediated by treatment-induced reduction of HIV viral 

replication as demonstrated by measurements of the amount of HIV RNA in the blood (the 

plasma viral load). However, successful suppression of HIV replication is influenced by the 

intrinsic potency of the prescribed regimen, patient adherence to treatment, and pre-existing or 

emerging resistance to antiretroviral (ARV) agents.2 

Resistance of HIV to ARV agents was first reported within 2 years of the approval of the 

NRTI zidovudine (ZDV) for the treatment of persons with late-stage HIV infection.3

Subsequently, transmission of a ZDV-resistant isolate was first reported in 1992.4

 The 

development of ARV resistance has since been reported with all other commercially available 

ARV agents within all classes.5

 Because drug resistance mutations often decrease the activity of 

many ARV agents within an individual class, the emergence of a single major resistance 

mutation can have important effects on a patient’s response to multiple ARV agents.5-7 Thus, 

assessment of the proportion of HIV-infected persons who have developed ARV resistance and 

characterization of the causes and factors associated with resistance development are critical 

steps in modifying treatment guidelines and regimens to improve their effectiveness. 

The emergence of mutations that confer resistance to ARV therapy is an expected 

consequence of the high rates of viral replication and the inherent error rate of the reverse 

transcription of single-stranded RNA viruses such as HIV.7 Among individuals who are 

receiving ARV, the likelihood of developing resistance is increased if optimal drug doses (that is, 

doses that reduce viral load to less than approximately 50 to 200 HIV RNA copies/mL)8,9 are not 

maintained, either through poor adherence or the prescription of a suboptimal regimen (such as 

the administration of single-dose neviripine [SD-NVP] to pregnant women infected with HIV for 

prevention of mother to child transmission [pMTCT] ). A second method of acquiring a resistant 

strain of the virus is via transmission of a resistant strain to a treatment-naïve person. 

The development of ARV resistance can be determined by the use of either genotypic or 

phenotypic assays.2,10 Genotypic testing assesses the viral genome for mutations in the genes 

that encode reverse transcriptase or protease; phenotypic testing assesses the ability of the virus 

to replicate in the presence of the drug in question. Interpretation of genotypic assays depends 

upon assessment of the probability that a given mutation pattern confers resistance to one or 

several specific ARV drugs.6

 Despite agreement regarding the significance of most individual 

mutations, experts continue to show some disagreement in the interpretation of genotypes.11 

Although the interpretation of phenotypic HIV resistance tests is straightforward compared with 

that of genotypic tests, these assays are considerably more expensive, and their clinical utility is 

less well validated by clinical trials.6

 

Both assays can be applied to virus obtained from any tissue, but for routine clinical 

purposes, the assays are used to characterize HIV in plasma specimens. Both tests are relatively 
2 

insensitive for the detection of resistant viral variants (or quasispecies) that account for less than 

20 percent of the circulating virus population in plasma, and neither assay detects intracellular, 

archival virus (virus that remains in a dormant state).6

 In contrast, by the use of specific genetic 

probes and allele-specific real-time polymerase chain reaction (PCR, a method used to amplify 

genetic material for sequencing or assaying), it is possible to detect viral subpopulations that 

constitute as little as 0.1 to 0.2 percent of circulating virus in plasma.12,13 

HIV gene mutations may be classified as primary or secondary. Primary mutations alter the 

binding of a drug to its target, resulting in increased amounts of medications necessary to inhibit 

the target enzyme. Secondary mutations increase the level of resistance by improving the fitness 

of the virus carrying the primary mutations. Often, secondary mutations have little or no effect 

on the level of resistance in the absence of primary mutations. Other genetic variations, called 

polymorphisms, are found frequently in untreated HIV positive populations in the developing 

world. A polymorphism is a form of genetic variation (specifically a discontinuous variation), 

which occurs in an animal species in which distinct forms exist together in the same population. 

(The human blood groups are examples of a polymorphism.) The interpretation of these 

naturally-occurring polymorphisms, usually found in HIV protease, is difficult. Generally, these 

variations are not primary mutations which confer significant resistance, but may be secondary 

mutations which could contribute to resistance or improve the fitness of resistant virus. 

Virologic treatment failure, and hence the emergence of ARV resistance, was particularly 

common in persons who received mono- or dual- drug therapy prior to the use of HAART 

regimens that included NNRTIs and PIs.14 As a consequence of prior inadequate therapy, the 

relatively poor potency of early HAART regimens, and poor adherence related to the complexity 

of dosing regimens and the frequency of adverse side effects, it was estimated that 50 percent of 

infected individuals who were receiving care for HIV infection in the United States (U.S.) in 

1999 had some evidence of ARV resistance.15 More recently, despite the development of new 

ARV agents with unique profiles of resistance mutations and regimens with less complex dosing 

and fewer side effects,2,10 ARV resistance remains a serious problem for HIV-infected 

patients.16,17 Furthermore, up to 10 percent of newly infected, treatment-naive individuals in the 

developed world are found to be infected by relatively fit, resistant virus that persists in the 

absence of treatment.18 

The purpose of this report was to review and synthesize the literature that describes the 

overall prevalence as well as factors in the development of ARV resistance throughout the 

developing world, particularly studies that address resistance in non-clade B viral strains (a clade 

is a group of organisms believed to originate from a single common ancestor; non-clade B 

viruses are that subtype of virus that is more common outside of North America and Western 

Europe). According to International AIDS Society recommendations,6

 evaluating susceptibility 

patterns among non-clade B persons should be a high priority because these viruses are by far the 

most prevalent world-wide. The first part of this report focuses on treatment-naïve populations in 

developing regions. The second focuses on the consequences of pMTCT regimens. Studies of 

pMTCT are particularly noteworthy, because they represent one of the most common uses of 

non-suppressive regimens of HAART. The third section focuses on adherence and its association 

with resistance. 
3 

Methods 

This project was suggested by the Fogarty International Center (Fogarty) at the National 

Institutes of Health (NIH) on behalf of several institutes at NIH, with the aim of guiding the 

research agenda on the development of ARV resistance in developing countries by identifying 

critical gaps in the published research. A secondary aim was to identify issues for clinicians 

rolling out HIV medications in the developing world. 

A technical expert panel (TEP) assisted in refining the methodology as well as the following 

key questions, which guided the review: 

1. What is the prevalence of resistance? Does the prevalence of resistance differ between 

adults and children? Between men and women? Between groups with differing modes of 

transmission? 

2. What are the factors associated with the development of resistance? How do the factors 

differ among varying population groups? 

3. What are effective strategies to prevent or reduce the development of resistance in 

different population groups (e.g., post pMTCT intervention; people receiving ARV)? 

4. What is the likely impact of low-level or partial resistance on subsequent therapy? What 

is the impact on response to subsequent pMTCT interventions? 

The literature search was initiated in November, 2005 with an electronic search of PubMed® 

and Embase as well as the Cochrane Controlled Clinical Trials Register Database and the 

Cochrane Database of Reviews of Effectiveness (DARE) for reports on resistance to ARV. 

Search terms included the generic and trade names of every available NNTRI, NRTI, Protease 

Inhibitor (PI), and fusion inhibitor (FI), regardless of U.S. Food and Drug Administration (FDA) 

approval status. Additional sources of evidence included the Stanford University HIV Drug 

Resistance Database; reports of WATCH: Worldwide Analysis of Resistance Transmission over 

Time of Chronically and Acute Infected HIV-1 infected persons; a recent presentation on 

pMTCT by a technical expert; a recent overview;18 and various conference proceedings. The 

Stanford HIV RT and Protease Sequence Database is an on-line relational database that catalogs 

sequence variation in HIV reverse transcriptase (RT) and protease enzymes, the molecular 

targets of anti-HIV therapy. One part of the database provides copies of or links to published 

papers, meeting abstracts, and GenBank entries that have not yet been published as a paper or 

abstract. 

Articles that did not report original research, that reported the results of animal or in vitro 

studies, that reported on case studies of fewer than 20 individuals, or that reported data already 

reported in another article were excluded (although we summarized the findings of several recent 

overviews). Although geographical setting was not initially considered a criterion for exclusion 

from the review, the TEP – after the first round of screening - recommended including only 

studies set in developing countries. The TEP also suggested that we focus on key questions one 

and two. 

Results for treatment-naïve populations and pregnant women and their children were 

examined separately. Because of study heterogeneity, pooling was not possible; thus, the data 

were summarized qualitatively. Differences by region, population group, and HIV viral clade are 

described. Resistance studies that reported adherence data are also summarized separately. 
4 

Results 

Of 1,122 titles identified by the literature search, only 117 met the inclusion criteria. 

Review of Published Overviews on Incidence and Prevalence 

Several overviews on the incidence and prevalence of ARV resistance were identified; 

however, most provided data only on the developed world. The WATCH study found that the 

rate of resistance (to any drug) was 5.5 percent in Africa, 7.4 percent in East Asia, 5.7 percent in 

Southeast Asia, and 6.4 percent in Latin America, lower than in North America (11.4 percent) 

and Europe (10.6 percent). The patterns of resistance world-wide appear to reflect trends in use 

of ARV medications: In developed areas, where medications have been more widely available, 

rates of resistance to NNRTI range from three to four percent, whereas, in developing regions 

with limited resources, the rates of resistance are much lower. 

Resistance Among Treatment-naïve Persons in Developing Countries 

We analyzed resistance prevalence separately for the following areas: India, other developing 

nations in Asia, Latin America, and the continent of Africa. 

Studies of ARV resistance among treatment-naïve patients in India were rare. Published data 

were found from only three studies;19-21 these studies varied in their results. A study of 60 

persons in Northern India found that at least 80 percent of patients had resistance to ZDV.19 A 

study of 50 persons in South India showed that fourteen percent were resistant to NNRTIs, 6 

percent were resistant to NRTIs, and 20 percent were PI resistant although all had mutations that 

conferred partial resistance.20 A study of 128 persons in Mumbai found that only two were 

resistant to NRTIs.21

Only three studies were found that reported on rates of resistance in other developing regions 

of Asia.22-24 None reported NNRTI resistance. NRTI resistance ranged from four to seven 

percent; primary resistance to PIs ranged from two to three percent. 

In Latin America, eight studies identified rates of ARV resistance. Resistance to NRTIs 

ranged from 2 to 14 percent among treatment-naïve groups.25-32 Reported rates of resistance to 

NNRTIs were low, ranging from zero to two percent. In a handful of studies that included 

Brazilian and Argentine populations, rates of secondary PI mutations were high, presumably 

among persons with HIV clade B. No studies assessed HIV resistance in Central America. 

In sub-Saharan Africa, 14 studies identified rates of ARV resistance among the treatment 

naive. NNRTI resistance rates ranged from 0 percent to 7.7 percent, and were associated with 

infection with most HIV clades.33-46 NRTI resistance rates ranged from zero percent to eight 

percent for all clades. Primary PI mutations were rare (less than three percent) among Africans; 

however, there were high levels of secondary PI mutations in most studies. 
5 

Resistance among Pregnant Women and Children in Developing 

Countries 

Thirty-one studies were identified that addressed the emergence of ARV resistance in women 

in developing countries subsequent to the administration of therapy to prevent pMTCT of HIV-1 

infection. These studies were highly heterogeneous with respect to study design and outcomes. 

Studies of resistance following SD-NVP. Seven studies assessed the effects of SD-NVP on 

postpartum NNRTI resistance; resistance rates ranged from 9 to 69 percent.47-53 Seven studies 

that assessed the effect of SD-NVP among women infected with clade C on resistance reported 

rates of prevalence that varied from over 70 percent at 2 weeks postpartum to less than nine 

percent at six weeks postpartum; these findings suggest a decline in resistance over time.49,52,54-58 

In studies of women infected with other clades,48,49,59-61 resistance ranged from 16 percent60 to 36 

percent.49

Complex patterns of NNRTI resistance were observed following the receipt of SD-NVP. 

The most common mutations that resulted in amino acid changes were K103N and Y181C. 

Y181C was the most commonly detected resistance mutation in plasma collected 2 weeks 

postpartum from women infected by HIV-1 clade C.54,55 In contrast, the K103N resistance 

mutation was most common at later time points in persons infected by clade C and at all times in 

persons infected by other HIV-1 clades. Among clade-C women, from one study in South 

Africa, V106/A/M was the most common amino acid change.54 One report found that the rates 

of detection of K103N, Y181C, and Y188C were significantly higher in women infected by 

HIV-1 clade C than by HIV-1 clades A or D.49

Several longitudinal analyses support the observation of declines in NNRTI resistance with 

time and suggest that these declines may differ by clade.47,48,52,55,62

Studies of resistance following other pMTCT regimens. Ten studies from the developing 

world were identified that studied the emergence of ARV resistance following other pMTCT 

regimens, including adding ARV therapy before or after SD-NVP. Two studies were done in 

Thailand,63,64 one was conducted in Argentina,65 and the other eight studies were done in SubSaharan Africa.50,60,66-71 A randomized comparison of outcomes in women receiving pMTCT 

with SD-NVP alone with those of women who received SD-NVP followed by a “tail” of 3 or 7 

days of ZDV and 3TC found that the prevalence of NNRTI resistance in these three groups was 

57 percent, 13 percent, and 9 percent, respectively.46

In one study, women who received either intrapartum SD-NVP or placebo following daily 

ZDV during their third trimester were put on three-drug ARV postpartum. Intrapartum SD- NVP 

was statistically associated with NRTI and NNRTI mutations at both 3 and 6 months. In another 

study, in which women were put on three-drug ARV after intrapartum SD-NVP or placebo, 

resistance was strongly associated with intrapartum SD-NVP among women who started ARV 

within 6 months postpartum, but not among women who started ARV 6 months or more 

postpartum,72 suggesting development of resistance may be associated with shorter interval 

between receipt of SD-NVP and initiation of full ARV. 

Several trials suggest that when infants receive SD-NVP at birth in the background of ZDV, 

maternal SD-NVP does not provide any additional protection from HIV transmission.71,73

Effect of test sensitivity. The rates of NNRTI resistance are consistently greater when 

more-sensitive assays are employed.51,58,65,74 For example, the prevalence detected with RT-PCR 
6 

(real time polymerase chain reaction) of plasma RNA can be up to double that detected with 

standard testing at six or seven weeks post-partum.

Resistance in HIV-positive Infants Born To Mothers Receiving pMTCT 

Children are often born HIV infected despite pMTCT. Resistant viruses can be transmitted 

or can emerge independently in either mother or infant. Eight studies50 54 55 57 60 62 69 75 evaluated 

the emergence of ARV resistance in children born to mothers in sub-Saharan Africa who 

received pMTCT. Most studies examined the impact of SD-NVP. In most studies, infected 

infants were tested for resistance at 6 or 7 weeks of age. Rates of NNRTI resistance among 

untreated HIV-positive infants of mothers receiving only SD-NVP ranged from 36 percent to 50 

percent. One study found that detectable resistance fades over time in infants exposed to SDNVP.62

Several studies compared the effects of multiple drugs on infant drug resistance. One study 

compared resistance rates among mother-infant pairs infected with various HIV clades who were 

treated with ZDV (N = 48) or SD-NVP (N = 61).60 The HIV transmission rates were similar in 

the two groups: 16.4 percent and 16.7 percent respectively. Using the oligonucleotide DNA 

ligation assay for resistance at 6 weeks postpartum, the researchers found NNRTI mutations in 

half the infected pairs who received SD-NVP. No ZDV mutations were present in pairs treated 

with that drug. Resistance data for mothers and infants were not presented separately. In a 

second study, researchers gave mothers ZDV (300mg) twice daily starting at 36 weeks gestation 

in addition to oral SD-NVP at onset of labor.69 Only 23 percent of their HIV-positive children 

were resistant to NNRTIs at 4 weeks postpartum. In a third study, researchers compared 

resistance among infants who received SD-NVP with those who received SD-NVP plus either 4 

or 7 days of ZDV + 3TC after birth.50 Infected infants who received the additional 7-day ZDV + 

3TC showed no resistance at 6 weeks, compared to 78 percent of those who received SD-NVP 

only. Finally, a fourth study recently compared resistance rates in infants who received various 

combinations of intrapartum SD-NVP, SD-NVP (2 mg/kg) immediately postpartum, and ZDV (4 

mg/kg) twice daily for one week.75 At 6 to 8 weeks, the rate of resistance was much lower (27 

percent) in the infants who received the postpartum SD-NVP and ZDV without the intrapartum 

SD-NVP. The study also showed that when infants received ZDV, the transmission rate did not 

differ between mothers who received SD-NVP and those who did not. When infants received 

SD-NVP plus one week of ZDV and the mother received SD-NVP, transmission was 17 percent 

and resistance was observed in 74 percent; when infants received SD-NVP plus 1 week of ZDV 

and mothers did not receive SD-NVP, transmission was 17 percent but resistance was only 27 

percent. Data from the MASHI trial also suggest that when the infant receives SD-NVP at birth 

in the background of ZDV, maternal SD NVP does not provide any additional protection.51 65 72 74

Predictors of Resistance. Several studies evaluated predictors of ARV resistance among 

persons receiving SD-NVP. A multivariate analysis demonstrated an increased risk of resistance 

detectable by standard genotyping assays in persons infected with clade C (compared with clade 

A or clade D) or with increased viral load at delivery, but not with increased age or number of 

births.49 One additional study supports the predictive value of increased viral load.54 Plasma 

HIV RNA level64 has also been shown to be predictive of resistance, and increased duration of 

prepartum use of ZDV+3TC for pMTCT was associated with an increased maternal prevalence 

of the M184V resistance mutation.76
7 

Adherence and Resistance 

Adherence to HIV treatment has long been associated with treatment outcomes. Most studies 

in the developed world have found evidence that at very low levels of adherence, there is 

insufficient selective pressure for mutations to evolve. At high levels of adherence, viral 

replication, and thus, viral evolution, should cease. 

Few studies could be identified that were designed to assess the effect of health services 

delivery factors or medication adherence on the development of resistance in patients in 

developing countries. Three studies assessed the impact of treatment interruptions on ARV 

resistance in the developing world: two were conducted in Kampala, Uganda.77 78 In the first 

study, 137 patients received a three-drug regimen; most included NVP (77 percent) or efavirenz 

(14 percent). At a median of 38 weeks, 91 of the 137 patients had undetectable viral loads. Of 

the 137 patients, 32 experienced an unplanned treatment interruption of more than 4 days. In 

multivariate analysis, this treatment interruption was statistically associated with resistance, as 

was being treatment-naïve at study entry. Of 36 patients for whom genetic data were available, 

26 were resistant to NNRTIs; the most common mutation was K103N. NRTI resistance was 

measured in 23 patients, attributable to the M184V/I mutation. A second study found that among 

95 participants, the 33 without treatment interruption had no drug resistance, compared to eight 

of the 62 participants who did interrupt treatment. A third African study that assessed the 

relationship between adherence and the presence of resistance in an Ivory Coast AIDS clinic 

found no association between missed treatments and resistance.79 Finally, one additional study 

from the UK studied black African children with non-clade B virus.80 All children whose 

adherence was classified as good or intermediate had resistance, compared with five of eight 

children whose adherence was poor. Of critical importance, unlike many studies conducted in 

the developed world, the latter studies were not initially designed or powered to assess the 

relationship between adherence and resistance. 

Discussion 

This review had several limitations. The primary limitation was the quality and quantity of 

available studies. Other limitations related specifically to how the studies were conducted, 

including heterogeneity with respect to study design, the lack of inclusion of participants infected 

with more unusual viral clades, and failure to stratify treatment-naïve patients. 

The paucity of quality research examining and characterizing ARV resistance among 

populations of developing nations leads us to make the following recommendations: 

Given the relatively high prevalence of HIV infection in India, more research on resistance 

patterns should be a priority for that nation. 

Few published studies stratified resistance data by host characteristics such as mode of HIV 

transmission, risk factors, or gender, although these data were collected in most of the studies. 

Studies with larger sample sizes would allow meaningful analyses of patterns among groups, for 

example MSM, heterosexuals, prostitutes, and IDUs. 

Data on HIV clades other than A, B, C, D, or the recombinant types were too scarce to permit 

reliable conclusions. In future studies, rare HIV clades should be over-sampled in order to 

provide statistically meaningful data. 

Evidence provided by longitudinal analyses suggests that the prevalence of NNRTI 

resistance may vary with the time elapsed since treatment among women taking SD-NVP for 
8 

pMTCT. In one study, fading of variants with Y181C was reported in women infected with 

clade A but not clade D; thus, Y181C may have less effect on viral fitness of clade D than on A. 

This observation warrants further investigation in future studies. The impact of the Y181C 

mutation should also be studied in clades other than D and A. 

 Research should be conducted regarding the need for maternal SD-NVP when an infant 

receives NVP at birth or when the mother receives ZDV regularly before birth. 

Further research is needed on the optimum time to begin ongoing postpartum ARV 

treatment. 

Where possible, future research projects on adherence should measure resistance in addition 

to routinely collected data such as CD4 count and viral load. In addition, observational studies 

of HIV treatment in developing regions should ask questions about factors that affect patient 

access to medication. 

More studies should use ultrasensitive assays to determine not just the occurrence of 

resistance but also the quantitative frequency of resistance mutations and types of mutations over 

time, which may be important in determining response to therapy. Where possible, patients, 

including mothers and their HIV positive children, should be followed over several years to 

assess the extent and quantity of archiving of resistance mutations in cells. 

Resistance surveillance programs should be established throughout the developing world. 

Data should be reported and analyzed in a consistent and timely fashion. It is expected that the 

Global HIV Drug Resistance Surveillance Network (HIV Resnet), recently launched by the 

World Health Organization, should fulfill this function. 
 

Evidence Report 
11 

Chapter 1. Introduction 

The clinical management of HIV infection has been greatly improved by the use of highly 

active antiretroviral (ARV ) therapy (HAART)1

 HAART comprises the following classes of 

agents: nucleoside or nucleotide reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse 

transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and fusion inhibitors. The clinical 

effectiveness of these therapies is mediated by treatment-induced reduction of HIV viral 

replication as demonstrated by measurements of the amount of HIV RNA in the blood (the 

plasma viral load). In turn, successful suppression of HIV replication is influenced by the 

intrinsic potency of the prescribed regimen, patient adherence to treatment, and pre-existing or 

emerging resistance to ARV agents.2

 

Resistance of HIV to ARV agents was first reported within 2 years of the approval of the 

NRTI zidovudine (ZDV) for the treatment of persons with late-stage HIV infection.3

Subsequently, transmission of a ZDV-resistant isolate was first reported 1992.4 The development 

of ARV resistance has since been reported with all other commercially available ARV agents 

within all classes.5 Because drug resistance mutations often decrease the activity of many ARV 

agents within an individual class, the emergence of a single major resistance mutation, e.g., the 

NRTI mutations M184V∗ or T215Y, the NNRTI mutation K103N, or any of a number of major 

PI mutations, can have important effects on a patient’s response to multiple ARV agents.5 Thus, 

assessment of the proportion of HIV-infected persons who have developed ARV resistance and 

characterization of the causes and factors associated with resistance development are critical 

steps in modifying treatment guidelines and regimens to improve their effectiveness. 

The emergence of mutations that confer resistance to ARV therapy is an expected 

consequence of the high rates of viral replication and the inherent error rate of the reverse 

transcription of single-stranded RNA viruses such as HIV.7 Because these mutations can 

decrease the growth rate or replication capacity of HIV,81 some drug-resistant viral strains do not 

compete successfully with wild-type virus in the absence of ARV therapy or the emergence of 

other compensatory mutations.7 However, whereas this phenomenon of decreased replication 

capacity has been demonstrated with some specific resistance mutations (e.g., K65R and 

M184V), other mutations such as the K103N mutations produce little if any impact on viral 

replication.82

In contrast, if non-suppressive antiretroviral therapy is administered, emergent resistant 

viruses are selected as the most replication capable (fit) virus and quickly predominate.83 In 

addition, prolonged non-suppressive ARV therapy may eventually select for the emergence of 

further compensatory mutations that increase fitness of resistant virus such that they compete 

successfully with wild-type virus even if ARV therapy is withdrawn. However, if ARV therapy 

is withdrawn prior to the emergence of compensatory mutations, overgrowth of more rapidly 

replicating wild-type viruses leads to subsidence of detectable resistant virus in the bloodstream 

within 4 to 6 weeks.84 Even so, resistant virus persists at low levels and/or in latently infected 

cells85,86 and may later re-emerge, often leading to the failure of subsequent therapeutic 

 

∗

 M184V refers to a mutation that results in the replacement of the amino acid methionine (M) with valine (V) at 

position 184. The one-letter amino acid abbreviations are as follows: A=alanine, C=cysteine, E=glutamic acid; 

G=glycine, I=isoleucine, K=lysine, L=leucine, M=methionine, N=asparagine, P=proline, V=valine, Y=tyrosine. 
12 

regimens.87 This phenomenon of re-emergence of drug resistance from cellular reservoirs has 

been best described in persons who have received prolonged courses of ARV therapy. Whether 

resistance that emerges after brief exposure (e.g., single-dose (SD) nevirapine (NVP) for 

preventing mother-to-child transmission (pMTCT) of HIV) has the same implications for the 

success of subsequent ARV therapy is less certain.88 

The plasma viral load directly correlates with the amount of viral replication and therefore 

serves as an indirect measure of the potential mutational rate of HIV and thus of the potential rate 

of acquisition of ARV resistance mutations. While any residual HIV replication during treatment 

may allow for continued viral evolution, the emergence of ARV resistance is unusual in persons 

who have isolated plasma viral loads no higher than 50 – 200 HIV RNA copies/mL.8,9 In 

contrast, failure to achieve intakes of HAART that are sufficient to maintain a plasma viral load 

of less than approximately 400 – 1,000 copies/mL is associated with an increased risk for 

developing ARV resistance.6,7 While patients may derive immunological and clinical benefit 

from a treatment regimen that does not fully suppress viral replication,8

 such patients remain at 

substantial risk for the eventual emergence of drug resistance mutations.89 

The observation of resistance in treatment-naïve individuals raises the question of when 

resistance testing should be conducted. This question is informed, at least in part, by the rate at 

which resistant virus is overgrown by wild-type virus. Because of the frequent, rapid subsidence 

of resistance when therapy is withdrawn, expert groups recommend that resistance testing should 

be done while patients are on therapy or shortly after the discontinuation of therapy,2,10 as testing 

can detect more mutations during this interval. In treatment-naïve patients or persons who have 

long since discontinued ARV therapy, resistance testing retains specificity but has decreased 

sensitivity. Nevertheless, the high rate of transmitted resistance has led to recommendations for 

testing chronically infected treatment-naïve persons. 

Frequency of ARV Resistance 

Virological treatment failure, and hence the emergence of ARV resistance, was particularly 

common in persons who received mono- or dual- drug therapy prior to the use of HAART 

regimens that included NNRTIs and PIs.14 As a consequence of prior inadequate therapy, the 

relatively poor potency of early HAART regimens, and poor adherence related to the complexity 

of dosing regimens and the frequency of adverse side effects, it was estimated that 50 percent of 

infected individuals who were receiving care for HIV infection in the United States (U.S.) in 

1999 had some evidence of ARV resistance.15 More recently, despite the development of new 

ARV agents with unique profiles of resistance mutations and regimens with less complex dosing 

and fewer side effects,2,10 ARV resistance remains a serious problem for HIV-infected 

patients.16,17 Furthermore, up to 10 percent of newly infected, treatment-naive individuals in the 

developed world are found to be infected by relatively fit, resistant virus that persists in the 

absence of treatment.18

Determination of ARV Resistance 

 The development of ARV resistance can be determined by the use of either genotypic or 

phenotypic assays.2,10 Genotypic testing assesses the viral genome for mutations in the genes 

that encode reverse transcriptase or protease; phenotypic testing assesses the ability of the virus 

to replicate in the presence of the drug in question. Both assays can be applied to virus obtained 
13 

from any tissue, but for routine clinical purposes, the assays are used to characterize HIV in 

plasma specimens. Both tests are relatively insensitive for the detection of resistant viral variants 

(or quasispecies) that account for less than 20 percent of the circulating virus population in 

plasma, and neither assay detects intracellular, archival virus (virus that remains in a dormant 

state).6 In contrast, by the use of specific genetic probes and allele-specific real time polymerase 

chain reaction (PCR, a method used to amplify genetic material for sequencing or assaying), it is 

possible to detect viral subpopulations that constitute as little as 0.1 to 0.2 percent of circulating 

virus in plasma.12,13 

 In clinically used genotypic assays, the sequences of the HIV-1 reverse transcriptase and 

protease genes are reverse-transcribed, and the resultant cloned DNA (cDNA) amplified and 

sequenced or otherwise assayed for known mutant sequences and compared to a list of mutations 

that have been associated with ARV resistance. An interpretive algorithm is then used to 

determine whether the identified mutations are likely to lead to decreased effectiveness of (i.e., 

resistance to) specific ARV agents. Interpretation of genotypic assays depends upon assessment 

of the probability that a given mutation pattern confers resistance to one or several specific ARV 

drugs.6 Despite agreement regarding the significance of most individual mutations, experts 

continue to show some disagreement in the interpretation of genotypes.11 Numerous schemes 

have been developed for interpreting HIV resistance genotypes. Since these schemes differ in 

how evidence regarding resistance is interpreted, in how interactions between mutations are 

weighted, and in the frequency with which they are revised in the light of new scientific 

evidence, it is not surprising that some of these schemes predict the phenotypic response to 

treatment substantially better than do others.90 

 Although the interpretation of phenotypic HIV resistance tests is straightforward compared 

with that of genotypic tests, these assays are considerably more expensive, and their clinical 

utility is less well validated by clinical trials.6 Phenotypic susceptibility assays report the drug 

concentration necessary to inhibit viral replication in vitro by 50 percent, the Inhibitory 

Concentration(IC)50. Traditionally, phenotypic assays for HIV drug susceptibility have required 

the preparation of a high-titer viral stock in tissue culture, followed by infection of a second 

culture and determination of the inhibitory effect of the agents in question. Such multistage 

assays are not only time-consuming and expensive, but the resultant values suffer from relatively 

poor inter-laboratory reproducibility.91 More rapid and reproducible viral phenotypic assays 

have been developed using recombinant DNA technology. In one such assay, the reverse 

transcriptase and HIV protease genes of a target virus are cloned and recombined with a 

laboratory HIV DNA clone from which the the reverse transcriptase and protease genes have 

been deleted. Another assay uses luciferase indicator genes to track the expression of genes that 

have conferred resistance.92, 93 

HIV gene mutations may be classified as primary or secondary. Primary mutations alter the 

binding of a drug to its target, resulting in increased amounts of medications necessary to inhibit 

the target enzyme. Secondary mutations increase the level of resistance by improving the fitness 

of the virus carrying the primary mutations. Often, secondary mutations have little or no effect 

on the level of resistance in the absence of primary mutations. Other genetic variations, called 

polymorphisms, are found frequently in untreated HIV positive populations in the developing 

world. A polymorphism is a form of genetic variation (specifically a discontinuous variation), 

which occurs in an animal species in which distinct forms exist together in the same population. 

(The human blood groups are examples of a polymorphism.) The interpretation of these 

naturally-occurring polymorphisms, usually found in HIV protease, is difficult. Generally, these 
14 

variations are not primary mutations which confer significant resistance, but may be secondary 

mutations which could contribute to resistance or improve the fitness of resistant virus. 

The purpose of this report is to review and synthesize the literature that describes the overall 

prevalence of ARV resistance throughout the world. We have emphasized studies conducted 

since 2000 and have particularly sought out studies in the developing world that address 

resistance in non-clade B virus (a clade is a group of organisms believed to originate from a 

single common ancestor; clade B viruses are that subtype of virus that is more common outside 

of the North America and Western Europe). According to the recommendations of the 

International AIDS Society,6

 evaluating susceptibility patterns among non-clade B persons 

should be a high priority because these viruses are by far the most prevalent worldwide. The first 

part of our report focuses on treatment-naïve populations in developing regions. The second 

focuses on the consequences of pMTCT regimens. Studies of pMTCT are particularly 

noteworthy, because they represent one of the most common uses of non-suppressive regimens 

of HAART. A third section reviews the few studies that report both adherence and resistance 

data. 

In these analyses, we examine whether the prevalence of resistance differs between adults 

and children, between men and women, and between groups with differing modes of 

transmission. We report factors associated with the development of resistance and how these 

factors differ among varying population groups. Factors of particular concern included viral 

clades (especially in the context of pMTCT studies in the developing world), region, treatment 

regimen, adherence, and host factors such as gender and mode of transmission. 
14 
15 

Chapter 2. Methods 

Original Proposed Key Questions 

This project was suggested by the Fogarty International Center (Fogarty) at the National 

Institutes of Health (NIH) on behalf of several institutes at NIH with the aim of guiding the 

research agenda on the development of ARV resistance in developing countries by identifying 

critical gaps in the published research. A secondary aim was to identify issues for clinicians 

rolling out HIV medications in the developing world. The following key questions were 

proposed: 

1. What is the prevalence of resistance? Does the prevalence of resistance differ between 

adults and children? Between men and women? Between groups with differing modes of 

transmission? 

2. What are the factors associated with the development of resistance? How do the factors 

differ among varying population groups? 

a. Viral factors 

b. Host factors 

c. Specific ARVs 

d. Resistance assay (whether resistance identified depends on the type of test used) 

e. Health service associated 

3. What are effective strategies to prevent or reduce the development of resistance in 

different population groups (prevention of Mother To Child Transmission (pMTCT); 

people receiving ARV, etc.)? 

4. What is the likely impact of low-level or partial resistance on subsequent therapy? What 

is the impact on response to subsequent PMTCT interventions? 

. 

Technical Expert Panel 

In designing the study questions and methodology at the outset of this report, the EPC 

consulted several technical and content experts. Broad expertise and perspectives were 

sought. The following scientists and clinicians participated in the TEP for this report: David 

Bangsberg, John Baxter, Lisa Frenkel, David Katzenstein, Shahin Lockman, Douglas Richman, 

Robert Shafer, Steve Spector, and Jonathan Uy. Appendix A∗

 provides a list of their names, 

degrees, and affiliations. 

Divergent and conflicting opinions are common and perceived as healthy scientific discourse 

that results in a thoughtful, relevant systematic review. Therefore, the final study questions, 

design, and/or methodologic approaches do not necessarily represent the views of all 

technical and content experts. 

The TEP’s participation in the preparation of the report began with a meeting conducted via 

conference call on February 27, 2006. The purpose of this meeting was to obtain TEP input on 

the scope of the project. The TEP expressed the strongly held belief that we focus on the ARV 

 

∗ Appendixes cited in this report are provided electronically at http://www.ahrq.gov/clinic/tp/antirettp.htm
16 

resistance picture in developing counties. During the course of the worldwide spread of HIV, the 

main virus (M) evolved into multiple clades. Most approved ARV medications were developed 

in studies of clade B, the most common clade in the Western world. Since clade B viruses 

account for only about 10 percent of HIV cases worldwide,94 knowledge of how ARVs affect the 

other clades is of critical importance. Thus, the TEP suggested that we provide an overview of 

the prevalence of resistance world-wide and how it differs by region. They asked us to address 

both resistance acquired through taking ARV drugs as well as drug resistance transmitted to 

treatment-naïve persons through infection. 

A second TEP meeting was held by telephone on May 26, 2006. To better match the scope 

of the project with resources, the panel agreed that we should focus on key question one and on 

parts a, b, c, and e of key question two. They expressed the belief that comparing types of 

resistance assays was beyond the scope of the project. They again emphasized the focus on 

developing countries. Specific concerns were MTCT and prevalence of ARV resistance in 

treatment-naïve populations. 

Literature Search 

Our search for studies began in November, 2005 with an electronic search of PubMed® and 

Embase for reports of resistance to ARV medications. We also searched the Cochrane Controlled 

Clinical Trials Register Database and the Cochrane Database of Reviews of Effectiveness 

(DARE). (The Cochrane Collaboration is an international organization that helps people make 

well-informed decisions about health care by preparing, maintaining, and promoting the 

accessibility of systematic reviews on the effects of heath care interventions.) 

We ordered all articles on resistance to ARVs, regardless of study design, language, or 

publication date. Search terms included the generic and trade names of every available NNTRI, 

NRTI, and Protease Inhibitor (PI), regardless of U.S. Food and Drug Administration (FDA) 

approval status. We also searched for studies of resistance to fusion inhibitors. We included only 

studies of humans; no animal studies or in vitro passage studies were included. Appendix B∗ 

shows our specific search terms. 

Additional Sources of Evidence 

Stanford University HIV Drug Resistance Database

The HIV RT and Protease Sequence Database is an on-line relational database that catalogs 

sequence variation in HIV reverse transcriptase (RT) and protease enzymes, the molecular 

targets of anti-HIV therapy. The database was developed in order to help physicians and 

researchers determine clinical cross-resistance among current and experimental anti-HIV drugs 

and to identify any drug regimens that retain their effectiveness against drug-resistant HIV-1 

isolates. The database links HIV-1 RT and protease sequence data, drug treatment histories, 

drug susceptibility, and clinical parameters. 

 

∗ Appendixes cited in this report are provided electronically at http://www.ahrq.gov/clinic/tp/antirettp.htm
17 

One part of the database provides copies of or links to published papers, meeting abstracts, 

and GenBank entries that have not yet been published as a paper or abstract. We searched the 

publications list in January, 2006, and downloaded relevant studies. We did not conduct our own 

analysis of the patient-level data stored in the RT and Protease Sequence database. 

WATCH: Worldwide Analysis of Resistance Transmission over Time 

of Chronically and Acute Infected HIV-1 infected persons 

 

Located in Europe, the WATCH project aims to collect HIV-1 RT and protease sequences 

from treatment-naïve participants all over the world and analyse them together in a standardised 

manner, in order to be able to make a good comparison of resistance figures. We found two 

WATCH conference abstracts and contacted the authors about additional research in progress. 

 

Presentation – Preventing Mother-to-Child HIV Transmission and ARV 

Drug Resistance 

Dr. Lynne Mofenson of the National Institute of Child Health and Human Development 

provided us with a copy of an overview she presented on March 16, 2006; this excellent 

overview contained nearly 100 slides, from which we obtained all relevant studies cited. 

Article – The Global Status of Resistance to ARV Drugs 

 

In 2005, Vella and Palmisano published an overview in the journal Clinical Infectious 

Diseases.18 They searched for published studies on the incidence and prevalence of drug 

resistance in persons recently infected with HIV in all regions of the world. We retrieved the one 

study from a developing country (Ivory Coast). 

We also searched the proceedings of the following conferences for the past 2 years. (We 

chose a 2 year cut-off because we expected that in general, abstracts and presentations would be 

published in journals within 2 years of the conference.) 

Conference on Retroviruses and Opportunistic Infections (CROI) 

The most recent CROI conference was held in Denver, Colorado on February 5-8, 2006. The 

CROI is a scientifically based meeting of leading HIV/AIDS researchers from around the world, 

and the 2006 conference was sponsored by the Foundation for Retrovirology and Human Health, 

the National Institute of Allergy and Infectious Diseases, the Centers for Disease Control and 

Prevention, and the University of California, San Diego School of Medicine. Participants 

included scientists actively engaged in basic science or clinical studies examining retroviral 

diseases and their complications or full-time academic clinician-teachers responsible for 

HIV/AIDS training and research programs. The aim of the conference was to enable researchers 

to present, discuss, and critique their investigations with the ultimate goal of translating their 

research into progress in the fight against HIV/AIDS. 
18 

International AIDS Conference 

 

The most recent International AIDS Conference was held in Toronto, Canada on August 13-

18, 2006. The conference is the largest HIV/AIDS meeting in the world; participants include 

scientists; health care providers; political, community and business leaders; journalists; 

government, non-governmental and intergovernmental representatives; and people living with 

HIV/AIDS. The goal of the conference is to allow for the exchange of ideas, research, and 

knowledge to help strengthen HIV/AIDS programs worldwide, with an emphasis on evidence, 

outcomes, and best practices. The theme of the 2006 conference was A Time to Deliver, 

underscoring the still urgent need to bring effective prevention and treatment programs to 

communities worldwide. 

IAS Conference on HIV Pathogenesis and Treatment 

 

The International AIDS Society (IAS) is a professional society with over 6,000 members, 

including scientists, health care workers, and others involved in the prevention and treatment of 

HIV/AIDS. Every 2 years, IAS sponsors a conference to disseminate knowledge that can 

accelerate the response to HIV/AIDS worldwide. We examined the proceedings from the July 

24-27, 2005 conference, which took place in Rio de Janeiro, Brazil and was co-sponsored with 

the Universidad de Federal do Rio de Janeiro and the Brazilian Society of Infectious Diseases. 

The specific aim of the conference was to focus on new insights into HIV disease development, 

prevention, and care and their practical applications in developing countries. 

Meetings of the Infectious Diseases Society of America (IDSA) 

 

The meetings of the Infectious Diseases Society of America (IDSA) are geared towards 

physicians, scientists, and other health care professionals involved in research, patient care, 

public health, disease prevention, and education in the field of infectious diseases (ID). The 

meetings are designed to disseminate current knowledge and advancements in the field, bridge 

the gaps among various medical disciplines, and promote multidisciplinary dialogues and 

communications that will facilitate the prevention and treatment of ID. The 2006 meeting of the 

IDSA took place on October 12-15 in Toronto, Canada, and included four program tracks: 

investigative infectious diseases (ID), adult ID, HIV, and pediatric ID. The IDSA website also 

provides a meetings archive that enabled us to examine the proceedings. 

Article Review 

Study Inclusion 

Our initial search was unrestricted by study design. The studies included in the review are of 

one of the following types of designs. 

Review articles identified by the search were classified as either systematic (including metaanalyses) or nonsystematic. Systematic reviews were identified by reading the methods section 

of the article to determine whether an acceptable method was employed to identify evidence 

(such as a description of the name of the computerized database searched and the full set of 
19 

search terms used, as well as details about the method for accepting and rejecting identified 

articles). 

Randomized controlled trials (RCTs) are studies where the participants are definitely 

assigned prospectively to one of two (or more) alternative forms of intervention, using a process 

of random allocation (e.g., random number generation, coin flips). 

Controlled clinical trials (CCT) s are studies where participants (or other units) are either 

(a) definitely assigned prospectively to one of two (or more) alternative forms of health 

care using a quasi-random allocation method (e.g., alternation, date of birth, patient 

identifier) 

OR 

(b) possibly assigned prospectively to one of two (or more) alternative forms of health 

care using a process of random or quasi-random allocation. 

Observational studies (such as cohort, case-control, and cases series) are those where the 

investigators do not control who gets the interventions. Much of the data included in this report 

comes from observational studies. To avoid reviewing potentially numerous case reports, we 

initially set a threshold of 50 or more participants per series for inclusion in our review. After 

discussion with our TEP, we reduced this number to 20 for studies of populations in developing 

countries, so as not to exclude potentially important data. 

Screening

Using a single-page “screening form” (included in Appendix C∗), we reviewed the studies 

retrieved from the various sources against our exclusion criteria. Two reviewers, each trained in 

the critical analysis of scientific literature, independently reviewed each study and resolved 

disagreements by consensus. The lead investigators resolved any disagreements that remained 

unresolved after discussions between the reviewers. 

To be included in our report, a study had to focus on human resistance to ARV. Studies of 

cell lines or animals were excluded. There were no language limitations; we included many nonEnglish studies Studies of obsolete therapies were also excluded at this time, if it was very 

unlikely that such therapies would never be used again, even in resource-limited regions. 

After the TEP further narrowed the scope of the project, we created a second one-page 

screening form. Using this form, we tracked articles on treatment-naïve patients, pregnant 

women and children. We also used this form to identify studies of entire geographic regions, 

large hospitals, and specific medications. 

During this phase of screening, we were asked to exclude studies not set in the developing 

world. “Developing” generally refers to economic growth and social development in areas such 

as health care, literacy, life expectancy, and fertility. Some less-developed regions could actually 

be considered non-developing, as a number have experienced years of decline rather than 

development. However, the United Nations (UN) allows each country to decide for itself 

whether it will be designated as “undeveloped” or “developing.” For the purposes of our report, 

we chose to include the following “undeveloped” and “developing” regions: Latin America, sub-

 

∗ Appendixes cited in this report are provided electronically at http://www.ahrq.gov/clinic/tp/antirettp.htm
20 

Saharan Africa, India, and all other areas of Asia except Hong Kong, Macau, Singapore, and 

Japan. 

Extraction of Study-Level Variables and Results 

We abstracted data from the articles that passed our screening criteria onto a specialized 

Quality Review Form (included in Appendix C∗

). The form collects data on geographic region, 

number of participants, subject demographics, HIV viral clade (clade), medications taken (if 

any), years of data collection, how people were selected for resistance testing, and how and when 

resistance was assessed. Data for all abstracted studies are presented in Evidence Tables 

(Appendix D). Trained reviewers, working in groups of two, extracted data from the same 

articles and resolved disagreements by consensus. A senior researcher resolved any 

disagreements not resolved by consensus. 

Synthesis of Results 

Results for a) treatment- naïve populations and b) pregnant women and their children are 

presented in separate tables. Because of study heterogeneity, pooling was not possible; thus, we 

summarize the data qualitatively. Differences by region, population group, and HIV viral clade 

are described. We also include a separate summary of resistance studies that reported adherence 

data. 

Peer Review 

A draft of this report was prepared in December, 2006 and sent to the TEP members and 

eight additional national and international experts for review. Peer reviewer comments were 

considered by the EPC in preparation of this final report. A list of peer reviewers and TEP 

members is included as Appendix A. Synthesis of the scientific literature presented here does not 

necessarily represent the views of individual reviewers. 

 

∗ Appendixes cited in this report are provided electronically at http://www.ahrq.gov/clinic/tp/antirettp.htm
21 

Chapter 3. Results 

Description of the Studies 

The literature search identified 1,122 titles. These references were culled from electronic 

library searches (510), conference proceedings (259), the Stanford University HIV Drug 

Resistance Database (141), and reference mining from retrieved articles (186). One content 

expert sent us an overview presentation on pMTCT. Twenty-five articles or abstracts were 

suggested by reviewers of a draft version of this report. 

Of the 1,122 titles identified as possibly relevant to our topics, 63 were excluded at abstract 

review and two could not be found, leaving 1,057 to be retrieved. Of these 1,057 articles, 

screening resulted in exclusion of 649 articles: 252 due to study design (background articles, 

commentary, individual case reports, case series of fewer than 20 persons); 220 focused on basic 

science or cell lines; 129 were excluded because the topic was not ARV resistance; and 48 

reported on obsolete therapies. The remaining 408 were then reviewed with a second screening 

form. 

Of these 408 articles, 291 were excluded from further analysis: 242 either because they were 

not within developing regions or not on pregnant women or children; 32 had no prevalence or 

incidence data; 14 reported the same data already reported in other included studies (duplicate 

data); and three had insufficient statistics. Data were abstracted from the remaining 117 studies 

(Figure 1 Literature Flow). 
22 

20 Not developing regions:

13 MTCT**

10 Children**

97 Developing regions:

31 Treatment Naïve**

31 MTCT**

29 Developing region / other**

17 infants**

Figure 1. Literature flow

117 Articles accepted to detailed review

510 Library Literature Search

1 Expert Presentation

259 Conference Proceedings*

141 Stanford Database

1122 Articles in Database

649 Rejected: 

252 Study design

220 Focus basic science/cell lines

129 Topic not ARV resistance

48 Obsolete therapies

1057 Articles Retrieved and Screened

65 Rejected:

63 Rejected at abstract

2 Not found

408 Articles Accepted to Second Screening

291 Rejected: 

161 Not developing region, mtct, children

81 Treatment naïve in developed regions

32 No prevelence or incidence data

14 Duplicate Data

3 Insufficient stats

* Including the Conference on Retroviruses and Opportunistic Infections (CROI), IAS 

Conference on HIV Pathogenesis and Treatment, International AIDS Conference and 

meetings of the Infectious Disease Society of America (IDSA).

** Categories not mutually exclusive. One article can contain data on treatment naïve 

patients, and/or MTCT

186 Reference Mining

25 Suggested by reviewers of Draft Report
23 

Published Overviews 

We found several overviews on the incidence and prevalence of resistance to ARV 

medications. Most focused on the developed world. 

Recent data on treatment naïve persons from ten large cities in the U.S.95 showed that 

resistance was higher in men who have sex with men (MSMs, 12 percent) compared to other risk 

groups and higher among whites (13 percent) than among other races. Overall, 8.3 percent of 

treatment-naïve persons were resistant to at least one drug. Regarding treatment-experienced 

patients in the U.S., 1998 data from the HIV Cost and Services Utilization Study (HCSUS) 

showed that 76 percent of viremic patients (that is, patients with measurable blood levels of the 

virus) were resistant to at least one drug. Of the viremic patients, 71.4 percent were resistant to 

NRTIs, 25.2 percent to NNRTIs, and 40.5 percent to PIs.15 In univariate analyses, men had a 

higher rate of resistance than women; there were no differences by race. Those with 

heterosexually acquired HIV or unknown mode of transmission had lower levels of resistance 

than MSMs and injection drug users (IDUs). The patterns likely reflect historical access to 

medications among population groups, that is, populations with earlier access to medications 

were more likely to be resistant. However, none of these variables were significant predictors of 

resistance in a multiple logistic regression that included CD4 count, viral load, and treatment 

variables. 

The CATCH study (Combined Analysis of Resistance Transmission over Time of 

Chronically and Acutely Infected HIV Patients in Europe) presented an overview of resistance in 

Europe. Authors analyzed data from 2,208 treatment-naïve individuals. Prevalence of resistance 

to any medication class was 10.4 percent: 7.6 percent were resistant to NRTIs, 2.9 percent to 

NNRTIs, 2.5 percent to PIs.96 97 Clade B viruses were more likely to carry resistance mutations 

than non-B clades (12.9 percent vs. 4.8 percent). Baseline resistance in new cases of non-B 

infection increased over time, from 2.0 percent in 1996-1998 to 8.2 percent in 2000-2001.

The WATCH study (described in the methods section) collected data on resistance from 

treatment-naïve participants from around the world. In 2006, researchers presented two 

abstracts{#2102}98 on 4,714 patients for whom the viral protease and/or reverse transcriptase 

sequences had been determined. The patients were primarily male (69 percent) with mean age 

35.3 years. Thirty-one percent of the patients identified as MSMs; another 9 percent were IDUs. 

Data on route of transmission were unavailable for 20 percent. Again, the rates of resistance 

reflect the patterns of drug availability over the course of the epidemic. The rate of resistance (to 

any drug) was 5.5 percent in Africa, 7.4 percent in East Asia, 5.7 percent in Southeast Asia, and 

6.4 percent in Latin America, lower than in North America (11.4 percent) and Europe (10.6 

percent). WATCH data suggest that the use of mono- and dual therapy in the developed world 

resulted in extensive transmission of NRTI resistance; Western regions had higher levels of 

resistance to NRTIs than to NNRTIs or PIs, whereas developing regions tended to have a 

relatively equal distribution of resistance over the three drug classes. Multi-class resistance was 

very low in both east and Southeast Asia (close to zero) compared to 3.1 percent in North 

America. The WATCH authors also calculated odds ratios - they were higher for NNRTI 

resistance in Africa (1.67) and Latin America (1.93) than in Europe, but these results did not 

meet conventional levels of statistical significance (p= 0.16 and 0.09, respectively). 

In 2005, a paper by Vella and Palmisano presented previously published data on the 

prevalence of resistance in recently infected persons in various countries. The analysis included 
24 

only one study from the developing world; it showed no drug resistance in 99 patients from 

Africa’s Ivory Coast. 

In sum, according to published overviews, the patterns of resistance world-wide appear to 

reflect trends in use of ARV medications. In developed areas, where medications were available 

to many HIV patients, rates of resistance to NNRTI ranged from three to four percent. In 

developing regions with limited resources, the rates of resistance were much lower among 

treatment naïve persons. Resistance to NRTIs ranged from seven to eight percent in the 

developed world. 

Treatment-naïve Persons in Developing Regions 

Tables 1 through 4 show the prevalence of drug resistance in treatment-naïve persons in 

developing countries. Because the studies are heterogeneous with respect to sample size, 

sampling criteria, selection for testing, type of assessment conducted, time from seroconversion, 

and population characteristics, they report conflicting results. Nevertheless, we believe this 

overview is an important starting point for discussion. 

Of the 30 studies retrieved, 25 reported clade data, although some of the studies grouped 

results from different clades together. Three studies included patients in India, three included 

patients across Asia, nine included patients in Latin America, and fifteen included patients in 

Africa. Data were collected between 1995 and 2004. The majority conducted genotypic testing 

only. 

India 

In recent years, ARV treatment in India has expanded. However, studies on resistance are 

quite rare. We found only three studies conducted in India that reported resistance in treatmentnaïve HIV positive persons, all published in peer-reviewed journals (Table 1). All studies 

conducted genotypic testing; none conducted phenotyping. None of the studies stratified data by 

mode of transmission, and none estimated time from seroconversion to resistance testing. Each 

study tested consecutive patients entering treatment. 

One study19 from North India assessed 60 men, women, and children from 2000-2002 using a 

sensitive nested amplification refractory mutation (ARMS) PCR test as well as a sequence-based 

mechanism. Of the NRTI mutations, about 32 percent occurred at codon 184, 80 percent at 

codon 70, and fewer than 2 percent at codon 215. NNRTI and PI mutations were not reported. 

Most participants showed a mixture of wild-type and mutant virus. CD4 count and gender were 

not statistically associated with mutations. Frequency of mutations at codon 70 was higher in 

adults than children. 

A second study20, collected data on 50 male and female adults in South India in 2002 and 

2003. All were infected with HIV clade C. Fourteen percent were resistant to NNRTIs and 6 

percent were resistant to NRTIs. The most common PI mutations were naturally occurring 

polymorphisms, including M36, L63, and I93. Twenty percent had PI mutations at major 

positions; the most common was V82. 

The final study collected data in 2003 from 128 participants in Mumbai (mean age 30.4 

years).21 Over 96 percent were infected with HIV clade C. Two participants were resistant to 
25 

NRTIs, as the M184V mutation was present. Polymorphisms such as M36 and L63 were 

common, but no major PI mutations were reported. 

In sum, the populations assessed were very small compared to the number of persons living 

with HIV in India. We are not sure how well they represent the regional populations. Results 

varied, and data were not usually stratified by variables of interest. More research on ARV 

resistance in India is recommended.
NR = Not reported 

26

Table 1. Treatment Naïve Data - India 

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI 

Sachdeva, 200519 India Children, women, men 2000- 2002 60 B,C NR Genotypic other, Nested PCR NR 31

184

215

Balakrishnan P, 

200520 India Women, men 2002- 2003 50 C NR 

Genotypic 

sequencebased 

mechanism, 

Nested PCR 

14% 

Deshpande A, 

200421 India Population NR 2003 128 (96.1%) C, (2.3%) A/C NR 

Genotypic 

sequencebased 

mechanism 

NR 
27 

Other Developing Nations in Asia 

We found only three studies that reported resistance patterns in treatment-naïve persons in 

other developing regions of Asia (we excluded Japan, Singapore, and Hong Kong) (Table 2). 

The first two studies did not stratify results by gender; none of the studies stratified by mode of 

transmission. All studies conducted genotypic testing; no phenotyping was conducted. All were 

published in peer-reviewed journals. 

The first study22 reported data for 50 adults, including MSMs and IDUs, in South Korea. 

Data were collected between 1998 and 2002. It is unclear how participants were selected for 

testing. Ninety-four percent of the sample was infected with HIV clade B. Participants were 

tested for resistance an average of 2 months after testing positive for HIV. None were resistant 

to NNRTIs, 6.5 percent were resistant to NRTIs, and 2.6 percent were resistant to PIs. The most 

common NRTI mutations were D67N, K70R, V118I, T215F, and T219Q. 

Another study23 reported data on 200 adults and adolescents in Vietnam; 42.5 percent were 

IDUs. Data were collected in 2001 and 2002. HIV clade was primarily CRF01_AE. None of the 

participants were resistant to NNRTIs; 4.5 percent were resistant to NRTIs, and 2.0 percent were 

resistant to PIs. The most common NRTI mutations were M41L, K219Q, and M184I. PI 

mutations found were D30N and L90M. 

 The last study24 collected data on all pregnant women (N = 124) and other adults (N=22) 

who consecutively entered a treatment program in Cambodia in 2003 and 2004. They were tested 

for resistance within 1 year of a known date of seroconversion. HIV clade was primarily 

CRF01_AE. NRTI mutations were found in 3.4 percent; the most common mutations were 

K70R, V75M, and K101E. Major PI mutations were found in two participants (1.4 percent); one 

had M46I, the other N88D. 

The samples in these studies were very small compared to the numbers of persons living with 

HIV in the region. Resistance data were not stratified by HIV risk factors, although that 

information was collected in at least two of the studies. Rates of resistance were fairly low 

among both clade B and recombinant clade CRF01_AE; rates were similar to those reported in 

Southeast Asia by the WATCH study.{Bowles, Wensing, et al. August 11-12 #2102}98 The 

specific mutations in the clade B South Korean participants were quite different from those 

found in the Southeast Asian CRF01_AE participants. 
NR = Not reported , IDU = Injection Drug User 

28 

Table 2. Treatment-Naïve Data – Other Nations of Asia 

Reference Country Population Data collected N Clade When assessed Type of assessment NNR

Park, S W, 

200322

South 

Korea 

IDU , MSM, 

women, other 

men 

1998-2002 50 94% B, 4% A, 2% G 

(median) 2 

months after 

HIV infection 

documented 

Genotypic 

sequencebased 

mechanism 

0% 

Lan N T, 200323 Viet Nam 

IDU, 

adolescents 

(12-18 yrs), 

women, men 

2001-2002 200 99% CRF01_AE NR 

Genotypic 

sequencebased 

mechanism 

NR 

Ly N, 200524 Cambodia Pregnant women, other 

adults 

2003-2004 146 99% CRF01_AE 

Known date of 

seroconversion 

of less than 1 

year 

Genotypic 

sequencebased 

mechanism 

NR 
29 

Latin America 

Nine studies reported data on resistance to ARV medications among treatment-naïve 

populations in Latin America. We found one study from Argentina, three from Brazil, one from 

Peru, one from Venezuela, and two from Mexico (one study99 combined data from several 

countries−Brazil, Portugal, Ivory Coast, Nigeria, Guinea Bissau, Lebanon, and the U.S. −but did 

not stratify data by region or HIV clade, so it was excluded). Data were collected between 1997 

and 2004. None of the studies reported time from seroconversion to assessment. The Peru and 

Argentina studies did not report HIV clade, nor did one of the studies from Mexico. None of the 

studies stratified resistance data by gender or mode of transmission, although one study included 

only MSM. All studies conducted genotypic assessment; two conducted additional phenotyping. 

Many studies did not report how participants were selected for resistance testing; statements 

were often vague as to whether all, or only a sample of patients entering treatment, were tested. 

The study from Argentina25 assessed resistance among adults, some of whom were IDUs. 

HIV clade was not reported. The authors compared persons with primary infection (N=13) to 

those with established infection (N=86). Of those with primary infection, one person was 

resistant to NRTIs and one was resistant to PIs. Of those with established infection, 1.2 percent 

had mutations to NRTIs and 1.2 percent had primary PI mutations (83.7 percent had secondary 

PI mutations). Line probe assays (LiPA), which identify specific mutations by a reverse 

hybridization strategy, were conducted on 52 of the established infection samples;100 11.5 

percent were resistant to NRTIs. 

In Brazil, a study of 409 treatment-naïve women (mostly infected with HIV clade C), MSMs, 

IDUs, and others showed very low resistance levels.26 Of the group, 2.06 percent were resistant 

to NNRTIs, 2.36 percent were resistant to NRTIs, and 2.24 percent were resistant to PIs. 

Another study of 49 adults, mostly infected with clade B HIV, reported that none were resistant 

to NNRTIs, 2.0 percent were resistant to NRTIs, and 85 percent had secondary PI mutations.27 

Another study of 50 adults (mostly infected with clade B), including MSMs, reported that 14 

percent were resistant to NRTIs and 85.7 percent had secondary PI mutations.28 The secondary 

mutations in these studies were most likely naturally occurring polymorphisms with no known 

relationship to resistance. 

A study of MSM in Peru29 compared resistance in 359 treatment-naïve and 16 treatmentexperienced patients. Resistance to drugs was low among the treatment naive – 3.3 percent 

overall, compared to 31.3 percent overall among the treatment experienced. HIV clade was not 

reported. 

A United Nations (UN) AIDS clinic in Venezuela30 reported data on adults including IDUs, 

MSM, and women. All but two persons had HIV clade B. The authors compared resistance rates 

of PI-naïve (N=56) and PI-experienced (N=44) patients. Some of the PI-naïve patients had 

experience with mono- and dual therapy. The rate of resistance was low among the PI naive – 

only one person was resistant to any drug. Among the PI-experienced patients, 40.9 percent were 

resistant to NRTIs and 9.1 percent were resistant to PIs. 

Finally, studies in Mexico reported that 5.0 percent of 20 adults infected with clade B who 

enrolled in treatment at a Jalisco clinic were resistant to PIs,31 while of 45 patients who enrolled 

for treatment in Central Mexico, 11.0 percent were resistant to NRTIs and 2.0 percent were 

resistant to PIs.32 Again, stratified data were not reported. 
30 

In sum, rates of resistance to NRTIs ranged from 2.0 percent to 14 percent among treatmentnaïve groups in Latin America. Rates of resistance to NNRTIs were low, ranging from zero to 

two percent. Rates of PI polymorphisms were high in Brazil and Argentina, presumably among 

persons infected with HIV clade B. Resistance data were rarely stratified by mode of 

transmission or gender, although those data were available in many cases. 

The number of persons tested for resistance in these studies is small relative to the number of 

people taking HIV ARVs in Latin America. Some studies tested all consecutive patients 

entering clinic26,29, while others did not explicitly state how participants were selected. 

Therefore, it is difficult to judge how representative the data are. We found no published reports 

of resistance rates in Central American countries, despite the high HIV prevalence rates in some 

of those nations. 
NR = Not Reported; IDU = Injection Drug Users; MSM = men who have sex with men; * represents primary PI mutations. 

31

Table 3. ARV resistance in treatment-naïve patients in Latin America 

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI 

Kijak, 200125 Argentina 

IDU, women, men - 

with established HIV 

infection 

1997-2000 86 NR NR 

Genotypic 

sequencebased 

mechanism and 

probe based 

system 

 

IDU, women, men - 

subset of above, 

with LiPA tests 

1997-2000 52 NR NR 

Genotypic 

sequencebased 

mechanism and 

probe based 

system 

 

IDU, women, men - 

with primary HIV 

infection 

1997-2000 13 NR NR 

Genotypic 

sequencebased 

mechanism and 

probe based 

system 

 

Dumans A T, 

200227 Brazil Population NR 1998 49 Mostly B NR 

Genotypic 

sequencebased 

mechanism 

0% 

Pires I L, 200428 Brazil Women, MSM 2000-2002 50 Mostly B NR 

Genotypic 

sequencebased 

mechanism 

 

Brindeiro R M, 

200326 Brazil Women, IDU, MSM 2001 409 (Mostly) C and F NR 

Genotypic 

sequencebased 

mechanism, 

Nested PCR 

2.06% 
32 

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI 

Lama, 200529 Peru Tx-naïve - MSM, other adults 2002-2003 359 NR NR 

Genotypic 

sequencebased 

mechanism 

 

Tx-experienced - 

MSM, other adults 2002-2003 16 NR NR 

Genotypic 

sequencebased 

mechanism 

 

AndradeVillanueva, 

200431

Mexico Women, men 2003-2004 20 B 

Genotypic 

sequencebased 

mechanism 

 

Delgado E, 

200130 Venezuela PI naïve; Women, IDU, MSM NR 56 Primarily B NR 

Genotypic 

sequencebased 

mechanism, 

Nested PCR 

1.80% 

 Venezuela PI treated; Women IDU, MSM NR 44 Primarily B NR 

Genotypic 

sequencebased 

mechanism, 

Nested PCR 

0% 

FuentesRomero, 200432 Mexico Population NR NR 45 NR at enrollment 

Genotypic 

sequencebased 

mechanism 

0% 
33 

Africa 

We found 14 studies that reported resistance data on treatment-naïve populations in subSaharan Africa. They are displayed in Table 4. Data were collected between 1995 and 2002. 

Studies were conducted in Cameroon, Senegal, Republic of Congo, Ivory Coast, Zambia, Gabon, 

Ghana, Malawi, South Africa, Zimbabwe, and Botswana; all reported HIV clade. The most 

common clades were CRF02 AG, which predominates in west Africa, and C, which is 

predominant in southern Africa. All studies conducted genotypic testing; three conducted 

additional phenotypic assessments33-35. Two studies included only pregnant women36,37; another 

included only men35. The other studies did not stratify results by gender. None of the studies 

stratified results by mode of transmission; the majority of studies described their participants as 

heterosexual adults. 

Of the studies that described participant selection, two studies38,39 tested random samples of 

patients, and one study tested all pregnant women entering a clinical trial.37 The other studies 

did not clarify how they selected participants for resistance testing. Many implied that all 

incoming HIV positive persons were tested; however, none explicitly stated this. 

Regarding treatment-naïve pregnant women, one study36 performed genotypic testing on 28 

women who entered treatment in Zambia in 2000; 92.8 percent of the women were infected with 

HIV clade C. None had any primary mutations; 89.3 percent had secondary NRTI mutations, and 

all had secondary PI mutations. Most secondary mutations were polymorphisms. Testing for RT 

mutations was also performed on samples from 37 pregnant women who entered a clinical trial 

in South Africa the same year.37 No women had resistance to NRTIs or NNRTIs; all were 

infected with clade C. 

The study that included only males35 found that although none of the 37 Ghanian men 

(mostly infected with mostly clade CRF02 AG) had primary PI mutations, secondary mutations 

were “commonly observed.” Exact figures were not reported. Testing for RT mutations was not 

performed. 

Two studies compared resistance among small samples of people infected with rarer HIV 

clades. Vergne40 reported data collected from 1995 to 1999 in Cameroon, Senegal, the Congo, 

and France. Regarding NNRTIs, one of five samples from participants infected with type J 

showed resistance, as did all four type O samples, compared to none of the type A, B, C, D, F, G, 

K, or recombinant types. Other than one participant infected with clade B, none of the others 

were resistant to NRTIs. No participants had primary PI mutations; all samples except those 

from participants infected with clade B and D had secondary PI mutations. Another study39

reported on resistance among participants infected with clades A, C, D, F2, G, H, and J in 

addition to the dominant CRF02-AG clade. Data were collected from adults and adolescents in 

Cameroon from 2000 to 2002. All samples had secondary PI mutations. Tests for RT mutations 

were not reported. 

Many of the studies conducted among individuals with highly prevalent HIV clades showed 

a high rate of secondary PI mutations in CFR02-AG. The same was true for HIV clade C. Rates 

of resistance to NNRTIs ranged from 0 percent to 7.7 percent in clade C-infected individuals and 

0 percent to 2 percent in those infected with CRF02-AG. Resistance to NRTIs also ranged from 

0 percent to 7.7 percent in clade C and from 0 percent to 5.1 percent in CRF02-AG. 

In summary, rates of NNRTI resistance ranged from 0 percent to 7.7 percent in most HIV 

clades. Prevalence was higher in clades B and O in one study, but samples were too small to 

allow generalization to the population at large. NRTI resistance rates ranged from 0 percent to 8 
34 

percent for all clades. Primary PI mutations were rare (<3 percent) among Africans. There were 

high levels of secondary PI mutations reported in most studies; there is no evidence that these 

affect resistance in the absence of primary mutations. It was unclear how some studies selected 

persons for genetic testing and most studies had small samples. Therefore, the generalizability of 

the data is limited. 
NR = Not Reported

35

Table 4. ARV Resistance Among Treatment-Naïve Patients in Africa 

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI NRTI Vergne L, 

200040

Cameroon

, Senegal, 

the 

Democrati

c Republic 

of Congo, 

France 

NR 1995- 1999 9 A NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 13 B NR 

Genotypic 

sequencebased 

mechanism 

0% 8% (primary) 

 NR 1995- 1999 2 C NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 5 D NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 11 F NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 4 G NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 2 K NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 5 J NR 

Genotypic 

sequencebased 

mechanism 

20% 0% (primary) 
36

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI NRTI Vergne L, 

200040 – 

cont’d 

 NR 1995- 1999 67 CRF02_A G NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 3 CRF01_A E NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 6 A/G NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 2 G/A/G NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 2 G/K NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 1 D/G/D NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 4 ?/K NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 2 unknown NR 

Genotypic 

sequencebased 

mechanism 

0% 0% (primary) 

 NR 1995- 1999 4 O NR 

Genotypic 

sequencebased 

mechanism 

100% 0% (primary) 
37

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI NRTI 

Petch L A, 

200541 Malawi NR 1996- 2001 21 C NR Genotypic sequence- based 

mechanism 

0% 

0%(major), 

100%(minor

) 

Toni T, 

200233 Ivory Coast 

Primarily 

men, 

heterosex

ual 

1997-

2000 99 

83% 

CRF02 

AG, 9% 

A, 4% 

CRF06 

median - 

9 mos 

from 

seroconv

ersion 

Genotypic 

sequencebased 

mechanism 

0% 0% 

Harrigan, 

200134

South 

Africa NR 1997 358 B and C NR Phenotypic VIRCO < 2% < 2% 

Laurent, 

200242 Senegal Women, men 1998- 2000 39 

Mostly 

CRF02_A

G, O, A, 

B, C, G, 

G/K 

Genotypic 

sequencebased 

mechanism 

 5.1% 

Handema R, 

200336 Zambia Pregnant women 2000 28 92.8% C NR 

Genotypic 

sequencebased 

mechanism 

0% 

89.3% 

(secondary), 

0% 

(primary) 

Konings F A, 

200439 Cameroon 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 14 A NR 

Genotypic 

sequencebased 

mechanism 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 77 CRF02- AG NR 

Genotypic 

sequencebased 

mechanism 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 3 C NR 

Genotypic 

sequencebased 

mechanism 
38

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI NRTI 

Konings F A, 

200439 - 

cont’d 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 8 D NR 

Genotypic 

sequencebased 

mechanism 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 4 F2 NR 

Genotypic 

sequencebased 

mechanism 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 8 G NR 

Genotypic 

sequencebased 

mechanism, 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 1 H NR 

Genotypic 

sequencebased 

mechanism 

Adolescen

ts (12-18 

yrs), 

women, 

men 

2000-

2002 7 J NR 

Genotypic 

sequencebased 

mechanism 

Vergne L, 

200243 Gabon Tx naïve adults 2000 13 CRF02_A G, A, G NR 

Genotypic 

sequencebased 

mechanism 

7.7% 7.7% 

ARV 

treated 

adults 

2000 19 CRF02_A G, A, D NR 

Genotypic 

sequencebased 

mechanism 

5.3% 78.9% 
39

Reference Country Population Data collected N Clade When assessed Type of assessment NNRTI NRTI 

Kinomoto M, 

200535 Ghana Adult males 2001- 2002 39 Most CRF02_A G 

Genotypic 

sequencebased 

mechanism, 

Phenotypic 

assay 

Bussman, 

200538 Botswana Women, men 2001 70 C NR 

Genotypic 

sequencebased 

mechanism 

2.00% 0% 

Toni T D, 

200344 Ivory Coast 

Pregnant 

women, women, 

men 

2001-

2002 

10

7 

(mostly)C

RF02_AG, 

A, K, 

CRF06_C

PX 

NR 

Genotypic 

sequencebased 

mechanism 

4% 1% 

Bessong P, 

200545

South 

Africa NR NR 40 C NR 

Genotypic 

sequencebased 

mechanism 

Doualla-Bell, 

200546 Botswana Tx-naïve adults NR 33 C NR 

Genotypic 

sequencebased 

mechanism 

PI-treated 

adults NR 15 C NR 

Genotypic 

sequencebased 

mechanism 

Pillay C, 

200237

South 

Africa 

Pregnant 

Women 2000 37 C 

Before 

entering 

clinical 

trial 

Genotypic 

sequencebased 

mechanism; 

Phenotypic 

assay 

0% 0% 
40 

Pregnant Women and Their Children in Developing 

Countries 

Overview 

We identified 31 studies in developing countries that addressed the emergence of ARV 

resistance in women subsequent to the administration of ARV therapy to prevent mother to child 

transmission (pMTCT) of HIV-1 infection. These studies were heterogeneous in terms of the 

duration of ARV treatment, the selection of the ARV regimen, the timing and frequency with 

which ARV resistance tests were done, the sensitivity of the assay for ARV resistance, and 

whether clade-specific data were reported. Many studies were reported only as conference 

abstracts; these studies tend to include less information than articles in peer-reviewed journals. 

In this section, we review the data on the prevalence of resistance in this group according to 

the prophylactic regimen, the infecting viral clade, the timing of the resistance assay (i.e., how 

long after the cessation of ARV therapy), and the assay that was used to detect ARV resistance. 

Resistance and pMTCT regimen 

Single dose Nevirapine (SD-NVP) alone. The greatest number of evaluable reports studied 

the impact of SD-NVP alone on the emergence of resistance (N= 14). Several of these reports 

provided data derived from the HIV-1NET 012 trial, which left three evaluable reports that 

provided non-overlapping data from the study,47-49 two reports that provided non-overlapping 

data from one South African study,50 51 and two reports that provided non-overlapping data from 

another South African study.52 53 All studies were done in sub-Saharan Africa. 

The earliest time that resistance was assessed was 7 days postpartum.47 Most studies 

assessed resistance 6 – 8 weeks postpartum (N = 10). Two studies evaluated the prevalence of 

resistance approximately 6 months postpartum. Eleven of the fourteen reports provided 

information by viral clade and three did not. The rate of NNRTI resistance 6 to 8 weeks post SDNVP ranged from 8.5 percent to 69.2 percent. 

Table 5 shows the results of standard genotypic resistance assays in the main evaluable 

studies. Studies that address specific questions in subpopulations of the main study (e.g., data 

comparing the results of highly sensitive assays for the detection of ARV resistance with 

standard genotypic resistance assays or studies of resistance over time13) are not included in this 

table. 
* 7% of isolates clade A

** 4 participants were not infected by HIV-1 clade C*** 1 subject infected by HIV-1 clade A

**** 23% of participants were infected by HIV-1 clades D, 3% by clade C and 15% by recombinant clades

a 61 women plus 10 infected infants; duration of NVP usage not clearly statedb 1% of participants were not infected by HIV-1 clade Cc 2% of isolates were not infected by HIV-1 clade C

41 

Table 5. NNRTI Resistance among pregnant women given single-dose nevirapine alone 

Reference Country When data collected N Clade When assessed (weeks post- partum) Typ

assess

Eshleman, 200548 Uganda 1997-1999 83 A 1 

Geno

seque

bas

mecha

Eshleman, 200548 Uganda 1997-1999 57 D 1 

Geno

seque

bas

mecha

Loubser, 200454 South Africa NR 35 Cb 2 

Geno

seque

bas

mecha

Kantor, 200355 Zimbabwe NR 28 C 2 

Geno

seque

bas

mecha

Toni, 200559 Cote d'Ivoire NR 29 CFR02-AG* 4 

Geno

seque

bas

mecha

Lehman, 2005101 Kenya NR 30 NR 4 

Geno

other, 

specif

PCR a

Mcintyre, 200550 South Africa NR 68 NR 6 

Geno

seque

bas

mecha

Loubser, 200658 South Africa NR 66 C*** 6 Geno

seque

bas
42

Reference Country When data collected N Clade When assessed (weeks post- partum) Typ

assess

mecha

Morris, 200356 South Africa 2002 141 C 6 

Geno

seque

bas

mecha

Gordon, 200457 South Africa NR 30 Cc 6 

Geno

seque

bas

mecha

Loubser, 200454 South Africa NR 164 Cb 6 

Geno

seque

bas

mecha

Troyer, 200560 Uganda NR 71a A  6 

Geno

other, 

labe

oligonu

ligation 

Martinson, 200452 South Africa NR 456 C**  7 Geno

other

Eshleman, 200549 Uganda 1997-1999 97 D 6 to 8 

Geno

seque

bas

mecha

Eshleman, 200549 Uganda 1997-1999 144 A 6 to 8 

Geno

seque

bas

mecha

Eshleman, 200549 Malawi 1997-1999 65 C 6 to 8 

Geno

seque

bas

mecha
43

Reference Country When data collected N Clade When assessed (weeks post- partum) Typ

assess

Kantor, 200355 Zimbabwe NR 32 C 8 

Geno

seque

bas

mecha

Eshleman, 200461 Uganda 1997-1999 28 Recombinant 6 to 8 

Geno

seque

bas

mecha

Author not available, 2003102 Zimbabwe NR 33 NR 8 Kantor, 200355 Zimbabwe NR 8 C 24 

Geno

seque

bas

mecha

Morris, 200453 South Africa NR 155 C** 26 

Geno

seque

bas

mecha
44 

Analysis of SD-NVP resistance data by clade. Thirteen studies of SD-NVP contrasted the 

emergence of ARV resistance in mothers infected by differing clades of HIV-1. Aside from clade 

C, for which 8 reports provided information regarding the emergence of resistance in seven 

clinical trials (data from one South African study of persons infected by clade C were provided in 

two reports52 53), no other clade was analyzed in more than two clinical trials. 

As shown in Table 6, the reported prevalence of NNRTI-resistance as assessed by 

standard genotypic resistance tests, is highly variable, ranging from over 70 percent at 2 weeks 

postpartum54 103 to 8.5 percent at 6 weeks postpartum in one study performed in South African 

women.56 Many studies showed a decline in resistance over time; this phenomenon will be 

discussed in more detail in a separate section. 
45 

Table 6. Resistance among pregnant women infected with HIV clade C after single-dose nevirapine 

Reference N Clade When assessed 

(weeks post-partum) 

Type of 

assessment 

NNRTI 

Resistance 

Loubser, 200454 35 C* 2 

Genotypic 

sequencebased 

mechanism 

71.0% 

Kantor, 200355 28 C 2 

Genotypic 

sequencebased 

mechanism 

75% 

Morris, 200356 141 C 6 

Genotypic 

sequencebased 

mechanism 

8.5% 

Gordon, 200457 30 C**** 6 

Genotypic 

sequencebased 

mechanism 

40.0% 

Loubser, 200454 164 C* 6 

Genotypic 

sequencebased 

mechanism 

48.0% 

Loubser, 200658 66 C*** 6 

Allele-specific 

real-time PCR 

assay 

54.0% 

Martinson, 200452 456 C** 7 Genotypic 

other, NR 38.8% 

Eshleman, 200549 65 C 6 to 8 

Genotypic 

sequencebased 

mechanism 

69.2% 

Kantor, 200355 32 C 8 

Genotypic 

sequencebased 

mechanism 

34% 

Kantor, 200355 8 C 24 

Genotypic 

sequencebased 

mechanism 

13% 

Morris, 200455 155 C** 26 

Genotypic 

sequencebased 

mechanism 

35% 

* 1% of participants were not infected by HIV-1 clade C

** 4 participants were not infected by HIV-1 clade C

*** 1 subject was infected by HIV-1 clade A 

****2% of participants were not infected by HIV-1 clade C
46 

Following SD-NVP, the prevalence of ARV resistance in women infected by HIV clades 

other than clade C ranged from 16 percent (6 weeks postpartum, clade A60) to 36 percent (6 – 8 

weeks postpartum, clade D47). A summary of results from studies of ARV resistance following 

administration of SD-NVP for pMTCT to women infected by other clades of HIV-1 is provided 

in Table 7. 

Table 7. ARV resistance after single-dose nevirapine, among women infected with other HIV clades 

Reference N Clade 

When assessed 

(weeks postpartum) 

Type of 

assessment 

NNRTI 

Resistance 

Eshleman, Sept 200548 83 A 1 

Genotypic 

sequence-based 

mechanism 

24.0% 

Eshleman, Sept 200548 57 D 1 

Genotypic 

sequence-based 

mechanism 

19.0% 

Toni, 200559 29 CFR02-AG* 4 

Genotypic 

sequence-based 

mechanism 

20.7% 

Troyer, 200560 71** A 6 

Genotypic other, 

Radio labeled 

oligonuc. DNA 

ligation (OLA) 

16.0% 

Eshleman, July 200549 144 A 6 to 8 

Genotypic 

sequence-based 

mechanism 

19.4% 

Eshleman, July 200549 97 D 6 to 8 

Genotypic 

sequence-based 

mechanism 

36.1% 

Eshleman, Feb 200461 28 Recombinant 6 to 8 

Genotypic 

sequence-based 

mechanism 

17.9% 

* 93% infected by CFR02-AG, 7% by clade A

** Resistance results are from 61 women plus 10 infected infants; 23% of patients were infected by HIV-1 clades D, 3% by 

clade C and 15% by recombinants

One formal cross-clade analysis of the prevalence of ARV resistance in female recipients 

of SD-NVP was identified. Using the results of the HIV-1NET 012 and NVAZ trials, Eshleman 

demonstrated that the proportion of women with clade C with at least one NVP resistance 

mutation (69 percent) 6 – 8 weeks postpartum was significantly higher than found in women 

infected by clade A (19 percent, p < 0.0001) or clade D (36 percent, p < 0.001).49 In the HIV1NET 012 trial, nevirapine resistance was greater in clade A than clade D. 

Specific NNRTI amino acid changes associated with resistance in persons receiving SDNVP. Complex patterns of NNRTI resistance were observed following the receipt of SD-NVP. 

The most common mutations that resulted in amino acid changes were K103N (lysine to 

asparagine at position 103) and Y181C (tyrosine to cysteine). Y181C was the most commonly 

detected resistance mutation in plasma collected 2 weeks postpartum from women infected by 
47 

HIV-1 clade C.54,55 In contrast, the K103N resistance mutation was most common at later time 

points in persons infected by clade C and at all times in persons infected by other HIV-1 clades. 

Among clade-C women from South Africa, V106/A/M (valine to alanine or methionine) was the 

most common amino acid change.54 One report found that the rates of detection of K103N, 

Y181C, and Y188C were significantly higher in women infected by HIV-1 clade C than by HIV1 clades A or D.49 Still, there has not been enough research to assess whether there are cladespecific differences in the prevalence of resistance. 

The findings from studies that provided data on the prevalence of various NNRTI resistance 

mutations are displayed in Table 8. 
* mothers also received ZDV for one month. Abbreviations: A=alanine, C=cysteine, E=glutamic acid; G=glycine, I=isoleucine, K=lysine, L=leucine, 

N=asparagine, P=proline, V=valine, Y=tyrosine. 

48 

Table 8. Specific mutations observed in mothers receiving single-dose nevirapine 

Proportion of women with specific, indicated resistan

Reference N Clade Weeks Postpartum Any K103N Y181C Y188C G190A V106A/M K101E 

Loubser, 200454 35 C 2 71% 29% 49% 34% 23% 43% Kantor, 200355 28 C 2 75% 25% 57% 14% 19% Loubser, 200454 164 C 6 48% 31% 23% 20% 14% 15% Gordon, 200457 30 C 6 40% 33% 10% 10% 3% 7% Eshleman, 2005,49 65 C 6 - 8 69% 58% 32% 17% 9% 3% 2% Kantor, 200355 32 C 8 34% 28% 6% 6% Eshleman, 2005,49 144 A 6 - 8 19% 17% 6% 1% 4% 1% 1% Eshleman, 2005,49 98 D 6 - 8 36% 29% 16% 3% 6% 0% 4% Toni, 200559 29 CRF02_AG 4 21% 10% 3% 3% Eshleman, 200461 28 Recomb 6 - 8 18% 14% 7% 4% Shapiro, 200671* 155 NR 4 45% 33% 8% 1% 5% 8% 
49 

Effect of single-dose nevirapine on resistance over time. A number of considerations 

suggest that the prevalence of readily detectable ARV resistance, particularly resistance that 

results from the use of NNRTIs, may vary after the discontinuation of ARV administration. 

First, significant serum concentrations of NVP may persist for prolonged periods of time after a 

single dose, leading to delayed (i.e., beyond 7 days) emergence of resistance. The prolonged 

presence of subtherapeutic serum concentrations may lead to ongoing selection of mutants for 2 

to 3 weeks. Conversely, if resistant virus is less fit than wild type virus, the prevalence of readily 

detectable resistant virus may gradually decline. Therefore, resistance testing done immediately 

after the administration of single dose NVP may underestimate the subsequent emergence of 

NNRTI-resistance due to this treatment strategy, whereas delayed ARV resistance testing may 

underestimate the prevalence of previously detectable resistance. 

Several studies, using a variety of assays including very sensitive ones, assessed the presence 

of NNRTI resistance over time among women who took SD-NVP to prevent mother-to-child 

transmission of HIV. Study data are presented in Table 9. 

Eshleman48 conducted genotypic testing on participants in randomized trial HIV-1 NET 012 

at 7 days postpartum. She found that 24 percent of women infected with HIV clade A had 

NNRTI resistance, compared to 19 percent of women infected with clade D. The same women 

were tested at 6 to 8 weeks postpartum. At that point, 28 percent of clade A women had evidence 

of resistance, compared to 42 percent of clade D women. The authors reported rapid fading of 

variants with Y181C in clade A but not in clade D. In the developed world, studies in 

individuals infected with clade B have shown that Y181C confers high-level resistance to NVP 

and impairs viral fitness. These results suggest that Y181C may have less effect on viral fitness 

of clade D than on fitness of clade A. Eshleman47 also did follow up on 11 women who had 

resistance at the 6- to 8-week time point. When genotyping was conducted between one and two 

years postpartum; none of the women had evidence of NNRTI resistance. 

Flys104 also reported recently on women from HIV-1 NET 012. (It is unclear how her sample 

overlaps with those in the previous publications.) She reported that 34.1 percent of 88 clade A 

participants had the K103N mutation at 6 to 8 weeks, compared to 53.6 percent of 56 clade D 

participants. Using follow-up tests and survival analysis, she estimated that the prevalence of the 

mutation declined to 3.6 percent in clade A and 29.8 percent in clade D at 2 years. By 4 years, 

she estimated that no clade A participants and only 2.4 percent of clade D participants had the 

mutation. 

The prevalence and decline of the most common NVP mutant, K103N, were also examined 

using allele-specific PCR in 65 women infected with HIV clade C in South Africa58 after SDNVP. The rate of resistance, assessed through a highly sensitive assay, declined steadily over 1 

year, from 87 percent at 6 weeks post-partum to only 11 percent at 1 year, according to RT-PCR 

of plasma RNA. PCR was used to detect cellular proviral DNA; these results were used to 

generate estimated rates of resistance of 52 percent at 6 weeks and only 4.2 percent at 1 year. Of 

note, the number of women available for testing at each follow-up ranged from 26 to 53 of the 

original 65. Samples were available at all time points for only 16 women. 

We also found two conference abstracts that assessed the association of resistance with time 

following SD-NVP in a pMTCT cohort. Martinson52 followed up on 456 women; all but four 

were infected with HIV clade C. NNRTI resistance was defined as any of the following 

mutations: K103N, V106 A/M, Y181C, Y188C, and G190A. It appears that each woman was 

tested once for resistance within 36 weeks of birth. Compared to women tested within 10 weeks 

postpartum, far fewer women who were tested between 10 and 36 weeks showed evidence of 
50 

resistance (44 percent versus 24 percent, respectively). Baseline CD4 cell count, viral load, time 

from birth to resistance testing, and number of times a mother took NVP during pregnancy were 

significantly associated with development of resistance. Martinson also measured resistance in 

infants;62 the results of this assessment are discussed below in the section on infants. 

Kantor55 assessed resistance over time in 34 women in Zimbabwe who received SD-NVP. 

All were infected with HIV clade C. NNRTI resistance rates dropped from 75 percent at two 

weeks postpartum to 34 percent at 8 weeks and 13 percent at 24 weeks. (The number of women 

available for testing dropped from 32 at eight weeks to only eight at 24 weeks, limiting the 

validity of the findings.) Prevalence of the Y181C mutation dropped from 57 percent at two 

weeks to six percent at week eight, while the K103N mutation was present in 25 percent of 

women at 2 weeks and 28 percent at 8 weeks. Similarly, Loubser54 studied a group of women in 

south Africa who had received SD-NVP; all but two were infected by HIV clade C. These 

investigators found that the prevalence of Y181C decreased from 49 percent at week 2 (N = 35) 

to 23 percent at week 6 postpartum (N = 164). The prevalence of the K103N mutation was 29 

percent at 2 weeks and 31 percent at 6 weeks. 

In sum, evidence provided by longitudinal analyses suggests that the prevalence of detectable 

NNRTI resistance may vary with time since treatment. Fading of variants with Y181C were 

reported in clade A but not in clade D. Prior studies show that Y181C confers high-level 

resistance to NVP and impairs viral fitness in persons infected by HIV clade B. Thus it is 

possible that Y181C may have less effect on viral fitness of clade D than of A. This observation 

warrants further investigation in future studies. 
a 35 patients were studied 2 weeks after delivery and 164 patients were studied 6 weeks after delivery 

b 2 patients were infected by HIV clade A 

51 

Table 9. Abatement of resistance over time in women taking single-dose nevaripine to prevent mother-to-child transmission 

Reference Country N HIV Clade Type of assessment NNRTI Resistance Resu

Martinson, 

200452 South Africa 456 C Genotypic other, NR 4-6 weeks 43% (N-unclear) 6-7 weeks 44% (N-unclear) 7-10 wee

(N-unc

Eshleman, 

200548 Uganda 65 A 

Genotypic 

sequence-based 

mechanism 

7 days 24% 6-8 weeks. 28% 

 D 

Genotypic 

sequence-based 

mechanism 

7 days 19% 6-8 weeks. 42% 

Eshleman, 

200147 Uganda 

311 in 

NVP 

arm 

A, D 

Genotypic 

sequence-based 

mechanism 

6-8 weeks 19% 

(21 of 111 

tested) 

12-24 mo

(of 11 of 

w/resistan

8 weeks

were re-

Flys, 2007104 Uganda 88 A Lig Amp assay 6-8 weeks 34.1% 2 years 3.6% 3 ye

1.3

 56 D Lig Amp assay 6-8 weeks 53.6% 2 years 29.8% 3 yea

18.9

Loubser, 200658 South Africa 67 C Allele-specific real-time PCR 6 weeks 87% (27 of 31 RNA tests) 3 months 65% (17 of 26 RNA tests) 7 months 

(14 of 36 

test

Kantor, 200358 Zimbabwe 34 C Genotypic sequence-based 

mechanism 

2 weeks 75% 

(21 of 28 tests) 

8 weeks 34% 

(11 of 32 tests) 

24 week

(1 of 8 

Loubser, 200454 South Africa 164a Cb Genotypic sequence-based 

mechanism

2 weeks 71% 

(25 of 35 tests) 

6 weeks 48% 

 (78 of 164 

tests) 
52 

Other pMTCT regimens, including therapy pre and post SD-NVP. Ten studies from the 

developing world were identified that studied the emergence of ARV resistance following other 

pMTCT regimens, including adding ARV therapy before or after SD-NVP. Two studies were 

done in Thailand,63,64 one was conducted in Argentina,65 and the other eight studies were done in 

Sub-Saharan Africa. The findings are presented in Table 9. 

In women using NRTIs alone,60,63,66,67 the rates of NRTI resistance ranged from zero to four 

percent. Rates of HIV transmission to infants varied by regimen. In a study of pregnant women 

taking ZDV and DDI from 36 weeks gestation, 5.4% of the infants were HIV positive. In two 

studies of ZDV alone, transmission rates were 16.5% and 16.7%. (In the former study, women 

were breastfeeding.) Another study of ZDV alone did not report transmission rates.

An RCT conducted in the U.S. and France (not displayed) assessed whether NVP resistance 

would occur after intrapartum NVP (or placebo) in women receiving standard ARV treatment 

during pregnancy.105 The study included mostly (62 percent) non clade B women, who were of 

African origin. 15 percent of the women in the NVP group developed a new NVP mutation at 6 

weeks postpartum. The development of a new NVP mutation did not correlate with CD4 cell 

count or viral load at delivery, or with the type of ARV after delivery. Similar trials were 

conducted in the developing world; rates of 32 percent and 33 percent for NNRTI resistance 

were observed in two trials using ZDV monotherapy in the pre-partum period followed by SDNVP during labor.69 In another study70 6.3 percent of women who took ARV followed by SDNVP showed NVP resistance at a mean of 48 days. A very recent study by Shapiro71 randomized 

pregnant women on ZDV-based ARV to either SD-NVP or placebo at birth. 45 percent of the 

SD-NVP group had NVP resistance at one month post-partum. Importantly, the difference in 

HIV transmission from mother to child was insignificant between the SD-NVP and placebo 

groups, suggesting that SD-NVP may be unnecessary in the context of ARV treatment of 

pregnant women 

The World Health Organization (WHO)’s revised guidelines recommend a combination 

of ZDV and lamivudine (3TC) at the “tail” end (post-partum) be used to reduce the risk of 

resistance from NVP.106 We found two trials that support these new guidelines. One prospective 

randomized trial compared the prevalence of NVP resistance in persons given SD-NVP followed 

by 0, 4 or 7 days of ZDV plus 3TC.46 The rates of NNRTI resistance in these three groups, as 

detected by standard genotypic resistance assays, were 57 percent, 13 percent, and 9 percent 

respectively. Similarly, in a non-controlled trial, Chaix et al. found that the rates of NNRTI 

resistance were less when SD-NVP was followed by the administration of ZDV plus 3TC for 3 

days post-partum than had been observed in previous trials of SD-NVP alone.68

Recent reports from sub-Saharan Africa indicate that risk of virologic failure (the failure 

to achieve measurable decreases in serum viral load after treatment) in women initiating ARV 

after SD-NVP is associated with the interval between receipt of SD-NVP and initiation of full 

ARV. Lockman72 showed that viral response was similar between women who had SD-NVP 

and those who received no SD-NVP (placebo) if they started treatment more than 6 months after 

SD-NVP, while viral failure was more common with SD-NVP if ARV was started less than 6 

months after exposure. The CD4 response was the same with or without SD-NVP, regardless of 

time of initiation. Data from Coovadia,107 where women started ARV a median of 2 years after 

SD-NVP exposure, found no difference in viral response between women with SD-NVP 

exposure and those without. Chi73 also found no difference between SD-NVP and no SD-NVP 

in viral response or CD4 count response. In this study, median time from SD-NVP to ARV 

initiation was 503 days; 81% started ARV at least six months post-partum. Additionally, several 
53 

abstracts have found that SD-NVP is as effective in second pregnancy as in first pregnancy.108 

109 None of these abstracts reported resistance rates. We strongly suggest that future studies of 

this nature include resistance testing. 

There are currently two RCTs funded by the NIH that will assess response to NNRTI- and 

PI-based therapy in persons with and without prior SD-NVP exposure. These trials, one in 

women and one in infants, will add significantly to our body of knowledge on this issue. 
* 14.5% of participants had NNRTI resistance mutations and 4.5% had NRTI resistance mutations prior to administration of 

pMTCT regimen; no new mutations emerged in any participant

** 3.5% of participants were infected by other HIV-1 clades

*** An unspecified minority of patients were infected by other HIV-1 clades

  4 persons were infected by clade B virus

** *** 23% of patients were infected by HIV-1 clades D, 3% by clade C and 15% by recombinants 

a ZDV and 3TC continued for 3 days post-partum

b All mothers had transmitted HIV-1 to their infants c ZDV & 3TC initiated during labor

d 24 women plus an unspecified number of infected infants e 21 (or 28?) women plus an unspecified number of infected infants

f 48 women plus 8 infected infants

54 

Table 10. Other pMTCT regimens, including pre- and post-SD-NPV therapy 

Reference Regimen N Clade 

When assessed 

(weeks postpartum) 

Type of 

assessment 

New 

NNRTI 

New 

NRTI 

Giuliano 2005b66 ZDV+DDI 22 NR 0 Genotypic 

other, NR 0%* 0%* 

Ekpini, 200267 ZDV 20 NR 0 

Genotypic 

sequencebased 

mechanism 

NA 0.0% 

Sutthent, 200563 ZDV 24d NR 0 

Genotypic 

sequencebased 

mechanism 

0.0% 0.0% 

Sutthent, 200563 ZDV+3TC 21e NR 0 

Genotypic 

sequencebased 

mechanism 

0.0% 0.0% 

Jourdain, 200464 ZDV 47 CRF01_AE** 1.5 

Genotypic 

sequencebased 

mechanism 

NA 4.0% 

Jourdain, 200464 ZDV + SD-NVP 209 CRF01_AE** 1.5 

Genotypic 

sequencebased 

mechanism 

32.0% 5.0% 

Chaix, 200568 ZDV+3TC+SDNVPa 96 CRF02*** 4 

Genotypic 

sequencebased 

mechanism 

1.1% 8.3% 

Chaix, 200469 ZDV+SD-NVP 74 NR 4 

Genotypic 

sequencebased 

mechanism 

33.0% NR 

McIntyre, 200550 SD-NVP 68 NR 6 

Genotypic 

sequencebased 

mechanism 

57.0% 0% 

McIntyre, 200550 SD-NVP+ 4 days 

ZDV & 3TC c 67 NR 6 

Genotypic 

sequencebased 

mechanism 

13.0% 0% 
55 

Reference Regimen N Clade 

When assessed 

(weeks postpartum) 

Type of 

assessment 

New 

NNRTI 

New 

NRTI 

McIntyre, 200550 SD-NVP+7 days 

ZDV & 3TC c 68 NR 6 

Genotypic 

sequencebased 

mechanism 

9.0% 0% 

Troyer, 200560 ZDV 56f A***** 6 

Genotypic 

other, Radio 

labeled 

oligonuc. DNA 

ligation 

0.0% 0% 

Lyons, 200570 ZDV-based HAART 32 Non-B (69%) 7 

Genotypic 

sequencebased 

mechanism 

6.3% 12.5% 

Shapiro, 200671 ZDV + SD-NVP 155 NR 4 

Genotypic 

sequencebased 

mechanism 

45% NR 

Perez, 200665 3TC+ZDV+NVP 20 B/F**** 12 

Genotypic 

sequencebased 

mechanism, 

Real time PCR 

0.0% 5.0% 
56 

Measuring the presence of resistance using standard vs. more-sensitive techniques. HIV 

resistance is usually assessed by performing population-based genetic sequencing of HIV RNA 

collected from virus found in plasma and determining the presence of specific mutations. These 

assays are insensitive to minor viral sub-populations that account for less than 20 – 30 percent of 

circulating virus. In contrast, by the use of specific genetic probes, RT-PCR, allele-specific PCR, 

or multiple single genomes, it is possible to detect viral subpopulations that constitute as little as 

0.1 – 0.2 percent of circulating virus in plasma. Other, more sensitive, assays include tests for 

the presence of HIV proviral DNA in mononuclear cells. 

As shown in Table 11, the rates of NNRTI resistance are consistently greater when moresensitive assays are employed.51,58,65,74 For example, Eshleman first reported rates of NNRTI 

resistance of 69.2 percent, 36.1 percent, and 19.4 percent, respectively for women infected with 

clade C, D, and A, 6 to 8 weeks after SD-NVP.49 According to Flys,110 Lig Amp assays on the 

same participants showed that in reality, 69.8 percent, 54.3 percent, and 41.7 percent of women 

with clade C, D, and A, respectively, had the K103N resistance mutation. 

Some of the studies also show the quantitative frequency of viruses with resistance as part of 

the quasispecies (closely related but non-identical mutant and recombinant viral genomes 

subjected to continuous genetic variation, competition, and selection; thought to be the 

mechanism by which RNA viruses persist).111 Loubser, 200658 showed that the actual frequency 

of resistant viruses is low and decreases further over time. Twenty seven of 31 women had the 

K103 N mutation at 6 weeks postpartum, but the median proportion of the virus that contained 

the K103N variant was 11 percent. At 3 months, in women who still had detectable resistance, 

the frequency was 6 percent; at 7 months, frequency was 1.2 percent; and at 12 months, the 

frequency was 0.7 percent. Thus, it is likely that time following SD-NVP exposure is very 

important in determining response to additional ARV therapy. 

 
* NNRTI resistance 

** NRTI resistance

a Loubser, 2006 (AIDS 2006; 20:995-1002), full publication of data in Loubser, 2005 b Patients received either 4 or 7 days of ZDV plus 3TC postpartum; substudy of McIntyre, 2005 c 61 mothers + 10 infected children 

d 48 mothers + 8 infected children e 23% of patients were infected by HIV-1 clades D, 3% by clade C and 15% by recombinants f Substudy of Martinson, 2004 g Detection of K103N resistance mutation only h 4 persons infected by clade B virus i Detection of K103N or Y181C resistance mutations j Detection of K70R resistance mutation only 

57 

Table 11. Standard versus more sensitive tests 

Reference N Regimen Clade When assessed (time post- partum) NNRTI Resistance 

Loubser, 2006a58 66 SD-NVP C 6 weeks 54.0%* stanLoubser, 2006a58 31 SD-NVP C 6 weeks 87.0%g* RT-PCLoubser, 2006a58 26 SD-NVP C 3 months 67.0%g* RT-PCLoubser, 2006a58 36 SD-NVP C 7 months 39.0%g* RT-PCLoubser, 2006a58 53 SD-NVP C 12 months 11.0%g* RT-PCLoubser, 2006a58 44 SD-NVP C 6 weeks 52.0%g* RT-PCR Loubser, 2006a58 48 SD-NVP C 48 weeks 4.2%g* RT-PCR Palmer, 200551 10 SD-NVP NR 6 weeks 50%* stanPalmer, 200551 10 SD-NVP NR 6 weeks 75%i* RT-PCPalmer, 200551 22 SD-NVP & ZDV+3TCb NR 6 weeks 0%* stanPalmer, 200551 22 SD-NVP & ZDV+3TCb NR 6 weeks 27%i* RT-PCTroyer, 200560 71c NVP Ae 6 weeks 16%* stanTroyer, 200560 71c NVP Ae 6 weeks 50%i* OligonucleoTroyer, 200551 56d ZDV Ae 6 weeks 0%** stanTroyer, 200560 56d ZDV Ae 6 weeks 0%j** OligonucleoJohnson JA, 2005f13 50 SD-NVP C 7 weeks 20%*g stanJohnson JA, 2005f13 50 SD-NVP C 7 weeks 52%*g RT-PCPerez, 200665 20 ZDV/3TC/NVP B/Fh 3 months 0%*g stanPerez, 200665 20 ZDV/3TC/NVP B/Fh 3 months 15%*g RT-PCEshleman, 200549 65 SD-NVP C 6 - 8 weeks 69.2%* stanEshleman, 200549 97 SD-NVP D 6 - 8 weeks 36.1%* stanEshleman, 200549 144 SD-NVP A 6 – 8 weeks 19.4%* stanFlys, 2006110 63 SD-NVP C 6 – 8 weeks 69.8%* L
58

Reference N Regimen Clade When assessed (time post- partum) NNRTI Resistance 

Flys, 2006110 94 SD-NVP D 6 -8 weeks 54.3%* LFlys, 2006110 144 SD-NVP A 6 – 8 weeks 41.7%* L
59 

Resistance in HIV-positive infants born to mothers receiving pMTCT. Children are often 

born HIV positive despite pMTCT. Resistant viruses can be transmitted or can emerge 

independently in either mother or infant. Eight studies50,54,55,57,60,62,69,75 evaluated the emergence 

of ARV resistance in children born to mothers in sub-Saharan Africa who received pMTCT. Most 

studies examined the impact of SD-NVP. Three studies reported on participants infected by HIV 

clade C; one other combined data from those with clades A, D, C, and recombinant types. The 

other studies did not report clade. 

We also found a study conducted in Thailand that reported 12-month postpartum resistance 

rates in children who, themselves, received ART for unspecified lengths of time.63 As the 

resistance could not be attributed to pMTCT alone, and specific pMTCT regimens were not 

mentioned, this study will not be discussed. 

In most studies, HIV-infected infants were tested for resistance at 6 or 7 weeks of age. Rates 

of NNRTI resistance among untreated infants of mothers receiving only SD-NVP ranged from 

36 percent to 50 percent. The most common mutations were Y181C and K103N. 

Martinson62 showed that detectable resistance fades over time in infants exposed to SD-NVP. 

Of the 53 HIV-positive infants studied, 45.3 percent had NNRTI resistance at their first visit 

(range 4 to 12 weeks). Those with resistance were tested again every 6 months. At 18 months, 

only one still had the Y181C mutation. 

Troyer60 compared resistance rates among mother-infant pairs infected with various HIV 

clades, who were treated with ZDV (N = 48) or SD-NVP (N = 61). The HIV transmission rates 

were similar in the groups: 16.4 percent and 16.7 percent respectively. Using a sensitive assay 

for ARV resistance (oligonucleotide DNA ligation assay) at 6 weeks, NNRTI mutations were 

found in half of the infected pairs who received SD-NVP. ZDV mutations were not present in 

pairs treated with that drug. Resistance data for mothers and infants were not presented 

separately. 

Chaix69 gave mothers ZDV (300mg) twice daily starting at 36 weeks gestation in addition to 

oral SD-NVP at onset of labor. Only 23 percent of their HIV-positive children were resistant to 

NRTIs at 4 weeks postpartum. McIntyre50 compared resistance among infants who received SDNVP with those who received SD-NVP plus either 4 or 7 days of ZDV + 3TC after birth. 

Infected infants who received the additional 7-day ZDV + 3TC showed no resistance at 6 weeks, 

compared to 78 percent of those who received SD-NVP only. 

Finally, Eshleman75 recently compared resistance rates in infants who received various 

combinations of intrapartum SD-NVP, SD-NVP (2 mg/kg) immediately postpartum, and ZDV (4 

mg/kg) twice daily for one week. At 6 to 8 weeks, the rate of resistance was much lower (27 

percent) in the infants who received the postpartum SD-NVP and ZDVwithout the intrapartum 

SD-NVP. The Eshleman study also showed that when the infant received ZDV, the transmission 

rate did not differ between mothers who received SD-NVP and those who did not. When the 

baby received SD-NVP plus one week of ZDV and the mother got SD-NVP, transmission was 

17 percent and resistance was seen in 74 percent; when the baby got SD-NVP plus 1 week of 

ZDV and the mother did not get SD-NVP, transmission was 17 percent but resistance was only 

27 percent. Data from the MASHI trial also suggest that when the infant receives SD-NVP at 

birth in the background of ZDV, maternal SD NVP does not provide any additional 

protection.72 As mentioned earlier in this report, Shapiro71 randomized pregnant women on 

ZDV-based treatment to either SD-NVP or placebo at birth; the difference in HIV MTCT 

between the SD-NVP and placebo groups was insignificant at one month. 
60 

These findings imply that research should be conducted into the need for maternal SD-NVP 

when an infant gets NVP at birth, or when the mother receives ZDV regularly before birth.
SD-NVP = Single dose Nevirapine 

ZDV = Zidovudine IP = Intrapartum * Resistance rates for mothers and infants combined 

61 

Table 12. Resistance in HIV positive infants born to mothers receiving pMTCT 

Reference Country Clade Regimen Type of assessment Re

Loubser, 200454 South Africa Mostly C SD-NVP Genotypic sequence- based mechanism 36% NGordon, 200457 South Africa C SD-NVP Genotypic sequence- based mechanism 40% NMartinson, 2004 & Morris, 200452 South Africa Mostly C SD-NVP 

Genotypic other; 

Genotypic sequencebased mechanism 42% NNRT

subgr

Troyer, 200560 Uganda A, C, D, recombinants ZDV Genotypic other, Radio labeled oligonuc. DNA ligation No 

A, C, D, 

recombinants SD-NVP 

Genotypic other, Radio 

labeled oligonuc. DNA 

ligation 

50% N

Chaix, 200469 Ivory Coast NR ZDV + SD-NVP Genotypic sequence- based mechanism 23% NMcIntyre, 200550 South Africa NR SD-NVP Genotypic sequence- based mechanism 78% N NR SD-NVP + 4 days ZDV+3TC Genotypic sequence- based mechanism 13% N NR SD-NVP + 7 days ZDV+3TC Genotypic sequence- based mechanism No Eshleman, 200675 Malawi NR Infant SD-NVP IP SD-NVP Genotypic sequence- based mechanism 87% NN

Infant SD-NVP+ ZDV 

IP SD-NVP 

Genotypic sequencebased mechanism 57% NN

Infant SD-NVP No IP SD-NVP 

Genotypic sequencebased mechanism 74% NN

Infant SD-NVP+ ZDV 

No IP SD-NVP 

Genotypic sequencebased mechanism 27% NN

Martinson, 200662 South Africa NR SD-NVP Genotypic sequence- based mechanism 45.2% NNR

4.2% 
62 

Predictors of resistance. Several studies evaluated the predictors of ARV resistance among 

persons receiving SD-NVP. In the most comprehensive analysis, a multivariate analysis 

performed by Eshleman and colleagues demonstrated an increased risk of resistance detectable 

by standard genotyping assays in persons infected with clade C vs. clade A or clade D, or 

increased viral load at delivery, but not with increased age or number of births.49 Similarly, 

Loubser found that an increased viral load was associated with an increased rate of resistance.54 

Jourdain also showed that plasma HIV RNA level was predictive of likelihood of ARV failure 

and NPV resistance.64

Chaix and colleagues found that increased duration of prepartum use of ZDV+3TC for 

pMTCT was associated with an increased maternal prevalence of the M184V resistance 

mutation.76 Another study50 found a decrease in the rate of NNRTI resistance with longer 

duration of ZDV+3TC post-partum. In both studies, SD-NVP was given during birth. 

The role of adherence in resistance is discussed in the next section.
63 

Adherence and Health Service Issues 

Adherence to HIV treatment has long been associated with treatment outcomes. Most studies 

in the developed world have found evidence that at very low levels of adherence, there is 

insufficient selective pressure for mutations to evolve. At high levels of adherence, viral 

replication, and thus, viral evolution, should be stopped. Recently, Bangsberg112 has suggested 

that the relationship between adherence and resistance differs for the three drug classes (NNRTI, 

NRTI, and PI). He also suggests that the different half-lives of medications play a significant role 

(in regard to mutations) when combination therapy is discontinued or interrupted. Thus, health 

service issues such as unreliable delivery, low stock, and financial constraints are important 

concerns in the development of ARV resistance in developing regions. 

We found three studies that assessed the impact of treatment interruptions on ARV resistance 

in the developing world; two of these took place in Kampala, Uganda.77 78 We also found 

another African study that assessed the relationship between adherence and the presence of 

resistance in selected populations.79 We found one additional study from the UK that studied 

black African children with non-clade B virus. Of critical importance, unlike many studies 

conducted in the developed world, the latter studies were not initially designed or powered to 

assess the relationship between adherence and resistance. 

The first study of treatment interruption included patients attending the HIV clinic at Mulago 

Hospital, Kampala, from August to December 2003. All patients received a three-drug regimen; 

most included NVP (77 percent) or efavirenz (14 percent). At a median of 38 weeks, 91 of the 

137 patients had undetectable viral loads. Of the 137 patients, 32 experienced an unplanned 

treatment interruption of more than 4 days. In multivariate analysis, this treatment interruption 

was statistically associated with virologic failure, as was being treatment-naïve at study entry. 

The most common reasons for treatment interruption were lack of money to buy medications (63 

percent) and toxicity/illness (31 percent). Of the 137 patients, 11 percent reported that, despite 

having money to buy medications, the medications were sometimes unavailable. 

Genotypic and phenotypic data were available from 36 of these patients with detectable viral 

load. Of these patients, 26 were resistant to NNRTIs; the most common mutation was K103N. 

NRTI resistance was measured in 23 patients, due to the M184V/I mutation. 

The second study in Kampala was a 24-week prospective observational study conducted 

between September, 2002 and April, 2004. Participants were recruited from pharmacies; they 

were on a generic fix-dosed combination, including NVP, lamivudine, and stavudine. Adherence 

was assessed through interviews, electronic medical monitors (EMMs), and unannounced visits 

to count pills. Treatment interruption was failing to open the EMM for at least 48 hours. 

Genotypic tests were conducted at 24 weeks. Adherence was good (82 percent - 95 percent) but 

declined significantly over time. At 24 weeks, 62 (65 percent) of the 95 participants with 

continuous EMM data had experienced at least one treatment interruption. Of the 33 participants 

without treatment interruption, none had drug resistance, compared to eight of the 62 participants 

who did have interruption. The most common mutation was Y181C. 

A UNAIDS clinic in the Ivory Coast tested all ARV treatment patients who had a rebound in 

plasma viral load between August, 1998, and April 1, 2000.79 Of these 97 patients, 86 had 

usable sequences. Thirty eight percent of the patients were female; the majority (89 percent) had 

A/G recombinant viruses. The rest were clade A, except for one clade G patient. Of the 86 

patients, 84 percent had received 2 drug therapies, and 15 percent had received 3 drug therapies 

that included a PI or NNRTI. Forty percent of the patients had interrupted therapy for at least 
64 

one day prior to resistance testing; the mean number of days interrupted was 36. Fifteen percent 

had switched drug regimens. Fifty percent reported missing a least one dose; the mean number of 

pills missed was six. 

 Seventy-nine percent of the 86 patients had genotypic resistance to at least one NRTI, 

NNRTI, or PI. Phenotypic resistance testing was conducted in 80 patients. Of these, 56 percent 

were resistant to at least one NRTI, 10 percent were resistant to at least one NNRTI, and 1.3 

percent were resistant to PIs. The authors conducted a logistic regression analysis of factors 

associated with drug resistance in patients with rebound in viral load, by comparing the 80 

patients with phenotypic and genotypic resistance to the 6 patients without evidence of 

resistance. The logistic model included variables for age group, gender, and various treatment 

characteristics. The variable “skipped pills” was not associated with resistance (adjusted OR = 

0.7, 95 percent CI 0.1 to 6.2). Likewise, “interrupt therapy ≥ 1 day” was not associated with 

resistance (adjusted OR = 0.3, 95 percent CI 0.1 to 2.9). The only variables associated with 

resistance were “use of dual therapy”(adjusted OR = 9.7, 95 percent CI 1.2-81.6) and the 

patient’s maximum initial plasma viral load response, measured at 30 days (adjusted OR = 2.8, 

95 percent CI 1.3-5.9). Given the small sample, confidence intervals are very wide, precluding 

conclusions about the relationship between adherence and resistance. 

In another study, researchers tested 80 patients enrolled in an initiative for access to ARV in 

Senegal113 between August, 1988 and February, 2001. The method of selection of these 80 

patients (almost equally split by gender) was not reported, except that patients had to have a 

biological follow-up of at least 6 months. The report also did not describe the degree to which 

these 80 patients represented the larger population of Senegalese with HIV. Among the patients 

studied, 68 were treatment-naïve at baseline. HIV clades were primarily recombinant forms. Of 

the patients, 66 received HAART and 14 received dual therapy. Median length of treatment at 

resistance testing was 18.4 months for those who were treatment-naïve at baseline and 30.0 

months for those who were treatment-experienced. Thirteen of the 80 patients were resistant to 

at least one NRTI, NNRTI, or PI. In bivariate analyses, the average monthly adherence for 

previously treatment- naïve patients did not differ significantly between resistant (n=8, 96.5 

percent) and non-resistant patients (n=60, 96.0 percent). In patients with prior ARV, adherence 

was 99.7 percent in both resistant (n=5) and nonresistant patients (n=7). In addition, adverse 

events that may cause adherence difficulties did not differ. Resistance also did not differ by 

gender, age, viral load, body mass index, or length of follow-up. Because of the small sample, 

no strong conclusions can be drawn. 

Researchers assessed the association between adherence and drug resistance in 26 children 

from a clinic in south London who had experienced virological failure between January, 1996, 

and June, 2000.80 These 26 patients were selected from 34 children who experienced one or 

more virologic failures during this same time and were part of a group of 105 HIV-1 infected 

children identified in South London. Twenty-four of the children were black African; 23 were 

infected with a non-B clade virus. Physicians reviewed medical records and estimated adherence 

for the six-month period prior to the onset of treatment failure. Adherence was categorized as 

good (>90 percent), intermediate (80-90 percent), or poor (<80 percent). 

HIV RNA sequence data were available for 21 of 26 children at treatment failure. Thirty 

three percent had resistance to PIs; 90 percent had RT mutations. Genotypic resistance was 

detected in ten of the eleven children who were treated with lamivudine, six of eight treated with 

NVP, and seven of eleven treated with ZDV. All children whose adherence was classified as 
65 

good or intermediate had resistance, compared with five of eight children whose adherence was 

poor. 

In summary, we identified few studies originally designed to assess the effect of health 

services delivery factors or medication adherence on the development of resistance in patients in 

developing countries. Results were mixed. Where possible, future research projects on 

adherence should measure resistance in addition to routinely collected data such as CD4 count 

and viral load. 
66 

Chapter 4. Discussion 

Limitations 

The primary limitations of this review are the quality and quantity of the available studies. 

Other limitations related specifically to how the studies were conducted, including heterogeneity 

with respect to study design, the lack of inclusion of participants infected with more unusual 

viral clades, and failure to stratify data on treatment-naïve patients by demographic or risk 

variables. 

The quantity of studies we were able to include was limited by the fact that we considered 

only studies whose results were published or were presented at major scientific conferences. Our 

search strategies were comprehensive, but it is possible we did not identify all published work. 

One function of the peer review process is to identify published studies we missed. In addition 

to the information obtained from published studies, it is possible that substantially more 

information regarding prevalence and predictors of resistance might have been available via new 

analyses of existing large datasets such as WATCH or the Stanford University HIV RT and 

Protease Sequence Database. 

The quality of the studies we identified was affected by two types of problems. The first is 

basic to all epidemiologic studies. Of high importance in studies that are primarily concerned 

with estimation – as are these studies of the frequency of resistance- is the representativeness of 

the studied population relative to some larger population of interest. In this case, the larger 

population of interest is usually something like “all treatment-naïve patients in the country [or 

some defined geographic area]” or “all patients infected with HIV clade C who have failed to 

respond to an initial treatment by time T with drugs X, Y, and Z.” Most identified studies either 

did not state how participants were selected for resistance-testing or spelled out methods that did 

not allow the reader to understand how representative the studied population was relative to a 

larger population of interest. Without such information, generalizing the results of identified 

studies to the inhabitants of a specific region is hazardous. The second problem is the small 

sample sizes of most of the identified studies, relative to the numbers of patients estimated to 

have HIV in the countries of interest. Given plausible assumptions regarding variability within 

populations, data derived from samples of 100 or 200 HIV-infected patients in a country with 

perhaps millions of infected persons cannot be extrapolated to that whole population with any 

confidence. 

The studies were heterogeneous regarding the timing and frequency of ARV resistance tests, 

the sensitivity of the assay for ARV resistance, and whether clade-specific analyses of ARV 

resistance were performed. This makes direction comparisons between groups difficult. The 

pMTCT studies were also quite heterogeneous in terms of the duration and type of ARV 

treatment. 

Data on HIV clades other than A, B, C, D, or the recombinant types were scarce. Only two 

studies which stratified results by clade reported data on clades F, G, K, J, and others. The 

samples were very small for those clades; the largest was 11 persons for clade F. Thus, results 

should be interpreted with caution. 

Finally, many studies of treatment naïve persons did not stratify the resistance data by 

variables of interest such as gender and mode of transmission, although that data was often 
67 

available. That being said, many sample sizes were small enough that stratification would have 

lacked statistical power to detect real differences. 

Conclusions and Recommendations for Future Research 

In Latin America, nine studies identified rates of resistance to NRTIs ranging from 2 to 14 

percent among treatment-naïve groups. Reported rates of resistance to NNRTIs were low, 

ranging from zero to two percent. In a handful of studies that included Brazilian and Argentinian 

populations, PI polymorphisms were common, presumably among persons with HIV clade B. 

We found no studies of HIV resistance in Central America. 

In Africa, studies identified NNRTI resistance rates from 0 percent to 7.7 percent associated 

with infection with most HIV clades. NRTI resistance rates ranged from 0 percent to 8 percent 

for all clades. Primary PI mutations were rare (<3 percent) among Africans; polymorphisms 

were widespread. 

We found published data from only three studies in India; these studies varied in their results. 

As India has a relatively high prevalence of HIV infection, more research on resistance patterns 

should be a priority. We found only three studies from other developing regions of Asia. None 

reported NNRTI resistance. NRTI resistance ranged from 4 to 7 percent; primary resistance to 

PIs ranged from 2 to 3 percent. 

Few published studies stratified resistance data by host characteristics such as mode of HIV 

transmission, risk factors, or gender, although these data were collected in most of the studies. 

Studies with larger sample sizes would allow meaningful analyses of patterns among groups, for 

example MSM, heterosexuals, prostitutes, and IDUs. In addition, data on HIV clades other than 

A, B, C, D, or the recombinant types were too scarce to permit reliable conclusions. In future 

studies, rare HIV clades should be over-sampled in order to provide statistically meaningful data. 

Evidence provided by longitudinal analyses suggests that the prevalence of NNRTI 

resistance may vary with time since treatment among women taking SD-NVP to prevent motherto-child transmission of HIV. In one study, fading of variants with Y181C was reported in 

women infected with clade A but not clade D. Y181C may have less effect on viral fitness of 

clade D than on A; this observation warrants further investigation in future studies. The impact 

of the Y181C mutation should also be studied in clades other than D and A. 

A randomized comparison of outcomes in women receiving pMTCT with SD-NVP alone, 

versus SD-NVP followed by a “tail” of 3 or 7 days of ZDV and 3TC found that the prevalence of 

NNRTI resistance in these three groups was 57 percent, 13 percent, and 9 percent, respectively. 

In a substudy of this trial, highly sensitive allele-specific RT-PCR assays detected the K103N 

mutation or Y181C resistance mutations in 75 percent of women receiving SD-NVP versus 27 

percent of women receiving SD-NVP plus 3 or 7 days of ZDV and 3TC. The ideal “tail” 

regimen and duration needs to be researched; drugs other than ZDV and 3TC could be studied in 

both mothers and infants. The use of a “tail” to prevent resistance needs to be evaluated with 

SD-NVP alone but also with SD-NVP plus a short course of ZDV, because resistance can occur 

even when ZDV is given. At least two trials evaluating the use of “tails” are currently in 

progress. 

In one study, women who received either intrapartum SD-NVP or placebo following daily 

ZDV during their third trimester were put on three-drug ARV postpartum. Intrapartum SD- NVP 

was statistically associated with virologic failure at both 3 and 6 months, as were NRTI and 

NNRTI mutations. In another study, in which women were put on three-drug ARV after 
68 

intrapartum SD-NVP or placebo, virologic failure was strongly associated with intrapartum SDNVP among women who started ARV within 6 months postpartum, but not among women who 

started ARV 6 months or more postpartum. Importantly, several trials suggest that when the 

infant receives SD-NVP at birth in the background of ZDV, maternal SD-NVP does not provide 

any additional protection. This finding should be researched further, as should the ideal time to 

start ongoing postpartum ARV treatment. 

We identified few studies designed to assess the effect of health services delivery factors or 

medication adherence on the development of resistance in patients in developing countries. 

Where resources permit, studies of adherence in developing regions should conduct resistance 

testing and report results. In addition, observational studies of HIV treatment in developing 

regions should ask questions about factors affecting patient access to medication. 

Studies using phenotype assessments were rare in developing regions. Funding of such 

studies is recommended due to their increased specificity. More studies should use ultrasensitive 

assays to determine not just frequency of resistance as “all or none” but also the quantitative 

frequency of resistance mutations and types of mutations over time, which may be important in 

terms of response to therapy. Patients, including mothers and their HIV positive children, should 

be followed over several years where possible, to assess the extent and quantity of archiving of 

resistance mutations in cells. 

Published data on resistance in developing regions, particularly India, Southeast Asia, and 

Central America, are scarce. Resistance surveillance programs should be established throughout 

the developing world. Data should be reported and analyzed in a consistent and timely fashion. 

To this end, the World Health Organization (WHO) recently launched the Global HIV Drug 

Resistance Surveillance Network (HIV Resent). 

The Stanford University database and the WATCH program based in the Netherlands collect 

resistance data from all over the world. It is critical that their data be continually updated and 

analyzed so that trends in resistant mutations can be recognized quickly and addressed. The 

WATCH program recently reported that only 58 percent of the researchers asked to share 

individual-level protease and RT sequences agreed. It is crucial that this level of collaboration 

be improved. 
69 

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72 

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Study, Abidjan, Cote d'Ivoire. 9. 2004:S176. 

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response and clinical outcomes on NNRTI-based 

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International AIDS Conference. Toronto, Cananda: 

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mutations arise in the majority of women provided 

single-dose NVP and appear to differ in emergence 

and persistence. Antivir Ther 2005; 10:S13. 

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Development of nevirapine resistance in infants is 

reduced by use of infant-only single-dose 

nevirapine plus zidovudine postexposure 

prophylaxis for the prevention of mother-to-child 

transmission of HIV-1. J Infect Dis 2006; 

193(4):479-81. 

 76. Chaix ML, Msellati P, Rouet F et al. Efficacy of 

Highly Active Antiviral Therapy and Rate of 

Genotypic HIV-1 Drug Resistant Strains among 

HIV-infected Children Receiving Treatment at the 

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patients attending a public, urban clinic in Kampala, 

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combination antiretroviral therapy in Kampala, 

Uganda. AIDS 2007; 21:1-7. 

 79. Adje-Toure C, Celestin B, Hanson D et al. 

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drug-resistant strains among patients who have 

rebound in viral load while receiving antiretroviral 

therapy in the UNAIDS-Drug Access Initiative in 

Abidjan, Cote d'Ivoire. AIDS 2003; 17 Suppl 

3:S23-9. 

 80. Mullen J, Leech S, O'Shea S et al. Antiretroviral 

drug resistance among HIV-1 infected children 

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 81. Coffin JM. HIV population dynamics in vivo: 

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therapy. Science 1995; 267(5197):483-9. 

 82. Havlir DV, Eastman S, Gamst A, Richman DD. 

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virus: kinetics of replication and estimated 

prevalence in untreated patients. J Virol 1996; 

70(11):7894-9. 

 83. Bangsberg DR, Acosta EP, Gupta R et al. 

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non-nucleoside reverse transcriptase inhibitors 

explained by virological fitness. AIDS 2006; 

20(2):223-31. 

 84. Deeks SG, Wrin T, Liegler T et al. Virologic and 

immunologic consequences of discontinuing 

combination antiretroviral-drug therapy in HIVinfected patients with detectable viremia. N Engl J 

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 85. Wong JK, Hezareh M, Gunthard HF et al. Recovery 

of replication-competent HIV despite prolonged 

suppression of plasma viremia. Science 1997; 

278(5341):1291-5. 

 86. Finzi D, Hermankova M, Pierson T et al. 

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highly active antiretroviral therapy. Science 1997; 

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 87. Benson CA, Vaida F, Havlir DV et al. A 

Randomized Trial of Treatment Interruption before 

Optimized Antiretroviral Therapy for Persons with 

Drug-Resistant HIV: 48-Week Virologic Results of 

ACTG A5086. J Infect Dis 2006; 194(9):1309-18. 

 88. Hammer SM. Single-dose nevirapine and drug 

resistance: the more you look, the more you find. J 

Infect Dis 2005; 192(1):1-3. 

 89. Barbour JD, Wrin T, Grant RM et al. Evolution of 

phenotypic drug susceptibility and viral replication 

capacity during long-term virologic failure of 

protease inhibitor therapy in human 

immunodeficiency virus-infected adults. J Virol 

2002; 76(21):11104-12. 

 90. De Luca A, Cozzi-Lepri A, Perno CF et al. 

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genotypic HIV-1 drug resistance and prediction of 

virological outcomes of the initial HAART by 

distinct systems. Antivir Ther 2004; 9(5):743-52. 

 91. Johnson VA. Nucleoside reverse transcriptase 

inhibitors and resistance of human 

immunodeficiency virus type 1. J Infect Dis 1995; 

171 Suppl 2:S140-9. 

 92. Hertogs K, Kemp S, Bloor S, et al. Patterns of 

cross-resistance among protease inhibitors in over 

1500 clinical HIV-1 isolates. Comparison of 

genotypic and phenotypic resistance profiles. 

Antiviral Ther. 1998; 3(Suppl 1):49-50. 

 93. Petropoulos CJ, Parkin NT, Limoli KL et al. A 

novel phenotypic drug susceptibility assay for 

human immunodeficiency virus type 1. Antimicrob 

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antiretroviral drug development. J Antimicrob 

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antiretroviral drug susceptibility among human 

immunodeficiency virus type 1 seroconverters in 

the United States, 1993-1998. J Infect Dis 2000; 

182(1):330-3. 

 96. Wensing AM, van de Vijver DA, Angarano G et al. 

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untreated individuals in Europe: implications for 

clinical management. J Infect Dis 2005; 192(6):958-

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 97. Wensing AMJ , Van de Vijver DAMC, Asjo B, et 

al. Analysis from more than 1600 newly diagnosed 

patients with HIV from 17 European countries 

shows that 10% of the patients carry primary drug 

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over Time of Chronically and Acute Infected HIV-1 

infected persons. 2006. 

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multiple mutations associated with protease 

inhibitor resistance in HIV-1. AIDS 2004; 

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 101. Lehman DA, Chung MH, Richardson BA, JohnStewart GC, Overbaugh J. Patterns of viral load and 

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 104. Flys TS, Donnell D, Mwatha A et al. Persistence of 

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8. 
A-1 

Appendix A. Technical Expert Panel Members and Peer 

Reviewers 

Technical Expert Panel Members 

Name Institution

David Bangsberg, MD University of California, San Francisco 

John Baxter, MD University of Medicine & Dentistry of New Jersey 

Lisa Frenkel, MD University Washington, Seattle 

David Katzenstein, MD Stanford University 

Shahin Lockman, MD Harvard School of Public Health AIDS Initiative 

Douglas Richman, MD University of California, San Diego 

Robert Shafer, MD Stanford Medical Center 

Steve Spector, MD University of California, San Diego 

Jonathan Uy, MD University of Illinois at Chicago 

In designing the study questions and methodology at the outset of this report, the EPC 

consulted several technical and content experts. Broad expertise and perspectives are 

sought. Divergent and conflicted opinions are common and perceived as health 

scientific discourse that results in a thoughtful, relevant systematic review. Therefore, in 

the end, study questions, design and/or methodologic approaches do not necessarily 

represent the views of individual technical and content experts.

Peer Reviewers 

Name Institution

Eric Daar, MD Harbor-UCLA Medical Center 

Dan Kuritzkes, MD Brigham and Women’s Hospital, Harvard Medical School 

Kenneth H. Mayer, MD Brown University 

William O’Brien, MD University of Texas Medical Branch 

Peer reviewer comments on a preliminary draft of this report were considered by the 

EPC in preparation of this final report. Synthesis of the scientific literature presented 

here does not necessarily represent the views of individual reviewers.
B-1 

Appendix B. Antiretroviral Drug Resistance – 

Search Methodology 

DATABASE SEARCHED& TIME PERIOD COVERED: 

PubMed – 1966-2005 

OTHER LIMITERS: 

HUMAN 

SEARCH STRATEGIES: 

SEARCH #1a (Protease Inhibitors) 

amprenavir OR tipranavir OR indinavir OR saquinavir OR lopinavir OR ritonavir OR 

fosamprenavir OR atazanavir OR nelfinavir) 

AND 

resistan* OR drug resistance, viral

TOTAL OF ABOVE SEARCHES: 974

SEARCH #1B (NNRTI’s) 

delavirdine OR efavirenz OR nevirapine 

AND 

resistan* OR drug resistance, viral

NOT 

Results of Search #1A 

TOTAL OF ABOVE SEARCHES: 374

SEARCH #1C (NRTI’s) 

zidovudine OR lamivudine OR emtricitabine OR abacavir OR zalcitabine OR tenofovir OR 

stavudine 

AND 

resistan* OR drug resistance, viral

NOT 

Results of previous searches 

TOTAL OF ABOVE SEARCHES: 1816

SEARCH #1D (Additional Drugs) 

didanosine OR enfuvirtide 

AND 

resistan* OR drug resistance, viral

NOT 

Results of previous searches 

TOTAL OF ABOVE SEARCHES: 507
Appendix C1. Abstraction Forms 

EPC Project: Resistance to Anti-retrovirals - Screener Form

C-1 

Citation: 

Reviewer: 

1. Does article study resistance to anti-retrovirals? 

(Circle one)

Yes......................................................1 

No .......................................................2 (STOP)

2. Does article focus on basic science, cell lines or 

animals exclusively? (Circle one)

Yes......................................................1 (STOP)

No .......................................................2 

3. Medication classes studied: (Check all that apply)

Non-NRTIs.........................................

NRTIs.................................................

Protease inhibitors ............................. 

Fusion inhibitors.................................

None of the above.............................. (STOP)

4. Study design: (Circle one)

Background (historical, editorial etc.) .....1 (STOP)

Non-systematic review .......................2 (STOP)

Systematic review / Meta-analysis ......3 (STOP) 

Case report/case series < 50 ..............4 (STOP)

Case series ≥ 50 .................................5 

Controlled trials...................................6 

Cohort .................................................7 

Case control........................................8 

Other...................................................9 (STOP) 

Case series ≥ 20 with children OR 

developing countries data......................10 

5. Population includes: (Check all that apply)

IV drug users......................................

Stimulant users ..................................

MSM ..................................................

Children (under 12 yrs old)....................

Adolescents (12-18 yrs old)..................

Pregnant women................................

Women (non-pregnant)......................

Adults NOS ........................................

Not reported.......................................

6. Region in which the study took place: 

 (Check all that apply)

US/Canada ........................................

Western Europe.................................

Eastern Europe..................................

Latin America.....................................

Australia/NZ .......................................

SE Asia/Indonesia..............................

India ...................................................

Other Asia..........................................

Africa..................................................

Not reported.......................................

7. Total sample size entering study. If entering 

sample not reported then total completing sample 

size: (Enter # or 999 if no sample reported)

 

8. Total duration of study: 

(For Duration enter # or 999 if not reported 

 and for units enter code from below.) 

Duration Units 

9. Language of article: (Circle one)

English................................................ 1 

Other................................................... 2 

Language (specify) : ________________ 

10. Do you think that this article might be a duplicate or 

include the same data as another study? (Circle one)

Yes ..................................................... 1 

No....................................................... 2 

If YES, which one(s) : 

________________________________ (Enter study ID #, author or 9999 if don’t know.) 

11. Is there a reference that needs to be checked? 

(Circle one)

Yes ..................................................... 1 

No....................................................... 2 

If YES, which one(s) : 

_____________________________________ 

(Enter reference # and/or author or 9999 if don’t know.) 

 ___ ___ ___ ___ ___ 

 ___ ___ ___ ___ ___ 

 Units

01. Hour 04. Month 

02. Day 05. Year 

03. Week 06. NR 

Notes: 
Appendix C2. Abstraction Forms 

EPC Project: Resistance to Anti-retrovirals - Level II Screener Form 

C-2 

Citation: 

Reviewer: 

1. Does the article report prevalence or incidence data 

about resistance in any of the following populations: 

(Check all that apply)

Treatment naïve patients.......................... 

Patients from all or almost all of a large 

geographically defined region, such as 

a country or part of a country.................... 

All patients from a large clinical practice, 

hospital, or similarly sized site .................. 

Patients receiving a very specific type 

of ARV, usually meaning in the context 

of a clinical trial......................................... 

None of the above ....................................  

2. Does the article report data specific to any of the 

subpopulations of interest as specified in the key 

questions for at least 70% of that population? 

(Check all that apply)

 IV drug users ............................... 

 Stimulant users .............................. 

 MSM .............................................. 

Children (under 12 yrs old) ............... 

Adolescents (12-18 yrs old).............. 

 Pregnant women............................ 

 Women (non-pregnant).................. 

 No specific data reported...............  

3. Does article report patient, virus, or treatment 

characteristics that are associated with the prevalence 

or incidence of resistance? 

 (Circle one)

Yes......................................................1 

No ......................................................2 

Notes: 
RAND-SCEPC Resistance to Antiretroviral Drugs Project 

Detailed Review Form 

 Page 1 of 6 

Article ID: Reviewer:______________ First Author: ____________________________________ (Last Name Only) Study Number: ___of____Description:________________ (Enter ‘1of 1’ if only one) (if more than one study) 1. In what region did the study take place? (CHECK ALL THAT APPLY) US/Canada................................... Western Europe ........................... Eastern Europe ............................ Australia/NZ................................ Middle East ................................. Latin America.............................. India............................................. Africa........................................... Asia : Japan .................................. Taiwan ............................... Singapore........................... Hong Kong ........................ Other Asia.......................... Not reported................................. 2. When was the sample collected? (Enter YEAR or YEAR RANGE. Enter 999 if not reported.) Year: ___ ___ ___ ___ Year Range: ___ ___ ___ ___ to ___ ___ ___ ___ 3. How was the cohort assembled: 

Clinical trial ......................................Other: Consecutive patients................

Convenience sample................

Random sample of larger databVolunteers, response to media 

Other method ....................................Assembly method not reported .........

4. What were the characteristics of the patie

Please check only if ≥ 70% of population for each of the following characteristics: 

A. Demographics: Men ....................................

Women ..............................

Adolescents (12-18 yrs old) Children (under 12 yrs old)

Caucasian ...........................African Ancestry ................Hispanic..............................Asian ..................................Native American ................Eskimo/Inuit.......................

Other (enter codes: _____________

Demographics not reported 

C-1
RAND-SCEPC Resistance to Antiretroviral Drugs Project 

Detailed Review Form 

 Page 2 of 6 

B. Modes of transmission: 

Injection drug use.....................................

MSM ........................................................

Heterosexual acquisition .......................... 

Peri-natal ..................................................

Contaminated blood products................... Mixed modes............................................ 

Other (enter codes:___________________________).  

Mode not reported .................................... 

C. HIV clade studied: 

(CHECK ALL THAT APPLY)

HIV-1 M Type: 

A1.....................................................

A2.....................................................

B....................................................... C.......................................................

D....................................................... E .......................................................

F1 ..................................................... F2 .....................................................

G.......................................................

H....................................................... I ........................................................

J........................................................

K....................................................... Mixed clade...................................... 

HIV clade not reported..................... 

HIV-1Other (enter codes: __________________).. 

HIV-1 Type not specified .................................. 

HIV-2 ................................................................. 

HIV Not otherwise specified ............................. 

OTHER (enter codes: _____________________) ......  

5. What was reported for the following ques

 subjects ages? (Enter number 99 for not report

Mean Age................................. ____ Median Age.............................. ____ Age Range................................ ____ 

6. Sample size data: 

(Enter number or 999 for not reported) Enrolled: _________ Followed up: _________ 

7. What were the study’s inclusion criteria? 

(Enter 

Enter code: ____ ____, ____ ____, _

____ ____, ____ ____, _

8. What were the study’s exclusion criteria? 

(Enter 

Enter code: ____ ____, ____ ____, _

 ____ ____, ____ ____, _

C-2 
RAND-SCEPC Resistance to Antiretroviral Drugs Project 

Detailed Review Form 

 Page 3 of 6 9. How were people selected for resistance testing? 

(CHECK ALL THAT APPLY)

Random sample.......................................................Entire population.....................................................Treatment failure..................................................... Other (enter codes: __________________________).. 

Selection method not reported ................................

10. How was resistance assessed? (CHECK ALL THAT APPLY)

Specific mutations:

NRTI (subclass code: ______________________). 

NNRTI......................................................... 

Protease inhibitors-Primary......................... 

Protease inhibitors-Secondary..................... 

Fusion inhibitors.......................................... 

Other (enter codes: ______________________________)

Genotypic resistance to specific drugs (enter codes).......  

Code(s): _________________________ 

Phenotypic resistance to specific drugs (enter codes) .....  

Code(s): _________________________ 

 Assessment not described ........................................  

11. What was the method of assessment? 

Genotypic: 

Sequence-based mechanism Probe-based system ..........Other (enter codes: ____________

Phenotypic:

VIRCO..............................Virologic...........................Other assay .......................

12. When was resistance assessed? 

At virological failure.........................At pre-set intervals............................Other (enter codes: _______________________

Assessment time not reported ...........

13. Did the study present an a priori statemen

Yes ....................................................No......................................................Predictors not described....................

C-3 
RAND-SCEPC Resistance to Antiretroviral Drugs Project 

Detailed Review Form 

 Page 4 of 6 14. Which predictors were analyzed? 

(CHECK ALL THAT APPLY)

Predictors not described............. Viral: 

Viral subtype...................... Super-infection .................. Other .................................. 

Host factors: 

MTCT intervention............ 

Mode of transmission ........ 

Immune status.................... 

Race ................................... Gender ............................... Other .................................. 

ARV...........................................

Health service associated ...........

Adherence ..................................

Other codes: _______________ 

15. Which analyses were run on the predictors listed in Q14?

(CHECK ALL THAT APPLY)

Univariate................................................................Multivariate............................................................. Analyses not described ...........................................

C-4 
RAND-SCEPC Resistance to Antiretroviral Drugs Project 

Detailed Review Form 

 Page 5 of 6 

EXPOSURE

16. Enter sample size and intervention/exposure data for each arm beginning with placebo or control, then in order of f

Arm/ 

Group Sample size Medications 

Continuous vs. Not continuous 

Time after 

discontinuation of TX Clade Type Duration of 

1 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

2 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

3 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

4 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

 Enter a number for N entering and N completing 

or enter 9999 if not reported. If observational study, circle appropriate unit of measurement: P Persons PY People years CNTRL Control CASES Cases 

Enter code(s) Enter # 

1. Continuous 2. Not continuous 8. NR 9. NA 

Enter a number for time or 997. Variable 998. ND 999. NA Enter a number for unit: 1.Hour 5. Year 2.Day 8. ND 3.Week 9. NA 4.Month 

Enter code(s) 99. NA if multiple clades 

Enter a number for t997. Variable 998. ND 999. NA Enter a number for u1.Hour 5. Year 2.Day 8. ND 3.Week 9. NA 4.Month 

C-5
RAND-SCEPC Resistance to Antiretroviral Drugs Project 

Detailed Review Form 

 Page 6 of 6 

EXPOSURE (continued)

 See instructions on previous page. 

Arm/ 

Group Sample size Medications 

Continuous vs. Not continuous 

Time after 

discontinuation Clade Type Duration of 

5 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

6 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

7 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

8 P 

PY __________________ CNTRL N ENTERINGCASES  __________________ 

N COMPLETING

______ ______ ______ ______ ______ ______ 

_____ 

Time: _______ Unit: _______ 

______ 

Time: _____Unit: _____

 Enter a number for N entering and N completing 

or enter 9999 if not reported. If observational study, circle appropriate unit of measurement: P Persons PY People years CNTRL Control CASES Cases 

Enter code(s) Enter # 

1. Continuous 2. Not continuous 8. NR 9. NA 

Enter a number for time or 997. Variable 998. ND 999. NA Enter a number for unit: 1.Hour 5. Year 2.Day 8. ND 3.Week 9. NA 4.Month 

Enter code(s) 99. NA if multiple clades 

Enter a number for t997. Variable 998. ND 999. NA Enter a number for u1.Hour 5. Year 2.Day 8. ND 3.Week 9. NA 4.Month 

C-6
D-1 

Appendix D. Evidence Table, Resistance to Antiretroviral Drugs in Regions 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1173 ADJE 20011 Design: Consecutive patients 

Sample Size: 81 Year/Range: 1998-1999 

Population: Adults (NOS), Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: ARV experienced 

SelectioTestingbased VIRCO 

1763 ANAWORANCIH 20062 Design: Clinical trial 

Sample Size: 125 Year/Range: 2002-2003 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: Western Europe, Australia/NZ, Other Asia 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: NR 

Selectio

STI-Tx Testingbased 

1968 ANAWORANICH 20053 Design: Clinical trial 

Sample Size: 348 Year/Range: NR 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: Western Europe, Australia/NZ, Other Asia 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve or Prior exposure to unboosted SQV regimen 

SelectioTesting

2088 ANDRADE- VILLANUEVA 

20044

Design: Case series, sample assembly NR Sample Size: 20 Year/Range: 2003-2004 

Population: Adults (NOS), Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 
D-2 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

2089 ANDRADE- VILLANUEVA 

20045

Design: Case series, sample assembly NR Sample Size: 50 Year/Range: 2002-2004 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Virological failure 

SelectioTestingbased 

1055 AUTHOR NOT AVAILABLE 

20036

Design: Case series, sample assembly NR Sample Size: 33 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: NR 

SelectioTesting

1944 AVERBUCH 20047 Design: Case series, sample assembly NR 

Sample Size: 59 Year/Range: NR 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Not Tx naïve Age/Range: NR / 1-18 Region: Western Europe 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Available information on ARV regimens, Viral load > 1000 copies/ml 

SelectioTesting

1627 BALAKRISHNAN 20058 Design: Case series, sample assembly NR 

Sample Size: 50 Year/Range: 2002-2003 

Population: Adults (NOS), Tx naïve Age/Range: 34 / 20-61 Region: India 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 

1582 BAUER 20019 Design: Clinical trial 

Sample Size: 81 Year/Range: 1994 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: US/Canada 

Med Class: NRTI Inclusions: ZDV resistance or Wild-type virus 

SelectioTesting
D-3 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1895 BESSONG 200510 Design: Case series, sample assembly NR 

Sample Size: 40 Year/Range: NR 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingPCR 

2102 BOWLES 200611 Design: Other 

Sample Size: 4714 Year/Range: NR 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Latin America, Africa, Asia 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Tx naïve 

SelectioTestingbased 

1533 BRENNER 200312 Design: Cohort, sample assembly NR 

Sample Size: 532 Year/Range: NR 

Population: Adults (NOS), Not Tx naïve Age/Range: NR / NR Region: US/Canada, Africa 

Med Class: Non-NRTI Inclusions: NR 

SelectioTestingbased VIRCO 

1633 BRINDEIRO 200213 Design: Cohort, sample assembly NR 

Sample Size: 52 Year/Range: NR/1999-2000 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Not Tx naïve Age/Range: NR / 2-14 Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Virological failure 

SelectioTestingbased VIRCO

1632 BRINDEIRO 200314 Design: Consecutive patients 

Sample Size: 535 Year/Range: 2001/NR-NR 

Population: IV drug users and men who have sex with men, and women, Tx naïve Age/Range: 31 / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 
D-4 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1634 BUSSMANN 200515 Design: Random sample of larger database 

Sample Size: 71 Year/Range: 2001/NR-NR 

Population: Adults (NOS), Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 

1468 CAROBENE 200416 Design: Cohort, sample assembly NR 

Sample Size: 583 Year/Range: NR 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Virological failure 

SelectioTestingbased 

1826 CHAIX 200517 Design: Clinical trial and random sample of larger 

database Sample Size: 112 Year/Range: 2002-2003 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Infected during birth, Transmitted HIV to child 

SelectioTestingbased 

1897 CHAIX 200518 Design: Case series, sample assembly NR 

Sample Size: 115 Year/Range: 2000-2003 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Not Tx naïve Age/Range: NR / 1-15 Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: ARV treatment ≥ 6 mo 

SelectioTesting

1950 CHAIX 200419 Design: Clinical trial 

Sample Size: 74 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: NR 

SelectioTestingbased 
D-5 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1152 CHANTRATITA 200220 Design: Case series, sample assembly NR 

Sample Size: 83 Year/Range: NR 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: Other Asia 

Med Class: NNRTI, Protease inhibitor Inclusions: ARV Tx with nucleosides, nonnucleosides, PIs, Acceptable compliance 

SelectioTestingbased 

1509 COHEN 200521 Design: Clinical trial 

Sample Size: 300 Year/Range: 2001-2002 

Population: IV drug users, and Adults (NOS), Not Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Eastern Europe, Latin America 

Med Class: Protease inhibitor Inclusions: Age ≥ 16 years, and Viral load > 1000 copies/ml, and Virologic response to at least1 HAART regimen, and Failure to prior regimen including at least 1 PI, and CD4 cell count > 50 cell/ mm3 

SelectioTesting

1290 COLGROVE 199822 Design: Convenience sample 

Sample Size: 48 Year/Range: 1989-1994 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: US/Canada, Latin America 

Med Class: NRTI Inclusions: Received ZDV Tx during pregnancy 

SelectioTestingbased 

1067 CUNNINGHAM 200223 Design: Clinical trial 

Sample Size: 217 Year/Range: 1997-2000 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Latin America 

Med Class: Non-NRTI Inclusions: Age ≥ 13 years, and > 20 weeks gestation, and Plasma RNA > 400 copies/ml 

SelectioTestingbased 
D-6 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1989 DEFORCHE 200524 Design: Other 

Sample Size: 940 Year/Range: NR 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Latin America, Africa, Japan, Other Asia 

Med Class: Non-NRTI, NRTI Inclusions: Received NVP-based ART 

SelectioTesting

1772 DELAUGERRE 200625 Design: Consecutive patients 

Sample Size: 53 Year/Range: 1997-2004 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Western Europe 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: NR 

SelectioTesting

1646 DELGADO 200126 Design: Cohort, sample assembly NR 

Sample Size: 100 Year/Range: NR 

Population: IV drug users, men who have sex with men, women, Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: NRTI, Protease inhibitor Inclusions: NR 

SelectioTestingPCR 

1647 DESHPANDE 200427 Design: Consecutive patients 

Sample Size: 128 Year/Range: 2003 

Population: Population NR, T Tx naïve Age/Range: 30 / NR Region: India 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, CD4 > 400 

SelectioTestingbased 

DOUALLA-BELL 200628

Design: Case series, sample assembly NR Sample Size: 23 Year/Range: 2002/NR-NR 

Population: Adults (NOS), Not TX naive Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Initiated NNRTI based-regimen, Claude C 

SelectioTestingbased 
D-7 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1995 DOUALLA-BELL 200529 Design: Cohort, sample assembly NR 

Sample Size: 48 Year/Range: NR 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: NR 

SelectioTestingbased 

1649 DUMANS 200230 Design: Other 

Sample Size: 49 Year/Range: 1998 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased VIRCO 

1297 EASTMAN 199831 Design: Clinical trial and random sample of larger 

database Sample Size: 96 Year/Range: 1993-1994 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: US/Canada 

Med Class: NRTI Inclusions: CD4 cell count > 200/μL, No indications for ARV Tx 

SelectioTesting
D-8 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1189 EKPINI 200232 Design: Clinical trial 

Sample Size: 84 Year/Range: 1996-1998 

Population: Pregnant women, Not Tx naïve Age/Range: NR / 17-37 Region: Africa 

Med Class: NRTI Inclusions: Received ZDV Tx during pregnancy, and Transmitted HIV to child, and Haemoglobin ≥70 g/L, and Absolute neutrophil count ≥1.0 X 

109/L, and ≥ 36 weeks gestation, and Platelet count >100 X 109/L, and Serum alanine aminotransferase concentration ≤ 2.5 times 

the upper limit of normal, and Serum creatinine concentration ≤150 g/L 

SelectioTestingbased 

ESHLEMAN 200633

Design: Clinical trial Sample Size: 329 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not TX naive Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Infant with known HIV status 

SelectioTestingbased 

1000 ESHLEMAN 200534 Design: Clinical trial 

Sample Size: 140 Year/Range: 1997-1999 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Age ≥ 18 years, > 32 weeks gestation 

SelectioTestingbased 
D-9 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1005 ESHLEMAN 200535 Design: Clinical trial and consecutive patients 

Sample Size: 306 Year/Range: 2000-2003 

Population: Pregnant women, Not Tx naïve Age/Range: 25 / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Expected delivery ≥ 4 hrs after enrollment 

SelectioTestingbased 

1042 ESHLEMAN 200436 Design: Clinical trial 

Sample Size: 279 Year/Range: 1997-1999 

Population: Pregnant women, Not Tx naïve Age/Range: 21-27 Region: Africa 

Med Class: Non-NRTI Inclusions: Age ≥ 18 years, > 30 weeks gestation 

SelectioTestingbased 

FLYS 200737

Design: Clinical trial Sample Size: 144 Year/Range: NR/1998-2003 

Population: Pregnant women, Not TX naive Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: K103N mutation present at 6-8 weeks 

SelectioTestingassay 

1932 FUENTES- ROMERO 

200438

Design: Case series, sample assembly NR Sample Size: 45 Year/Range: NR 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, Age > 14 years 

SelectioTestingbased 

1653 GALLANT 200439 Design: Clinical trial 

Sample Size: 602 Year/Range: 2000-2004 

Population: Pregnant women, and adults (NOS), Tx naïve Age/Range: 38 / 18-64 Region: US/Canada, Western Europe, Latin America 

Med Class: Non-NRTI, NRTI Inclusions: Viral load > 5,000 copies RNA/ml, Antiretroviral naïve 

SelectioTestingbased Virolog
D-10 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1829 GIULIANO 200540 Design: Clinical trial 

Sample Size: 47 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Infected during birth, Transmitted HIV to child 

SelectioTesting

1918 GORDON 200441 Design: Case series, sample assembly NR 

Sample Size: 60 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Received PMTCT 

SelectioTestingbased 

1470 HAN 200542 Design: Cohort, sample assembly NR 

Sample Size: NR Year/Range: 2003 

Population: Population NR, Not Tx naïve Age/Range: NR / 23-54 Region: Other Asia 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: CD4 < 350 

SelectioTestingbased 

1658 HANDEMA 200343 Design: Case series, sample assembly NR 

Sample Size: 28 Year/Range: 2000 

Population: Pregnant woment, Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 

1820 HANLON 200644 Design: Cohort, sample assembly NR 

Sample Size: 65 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Western Europe 

Med Class: NRTI, Protease inhibitor Inclusions: NR 

SelectioTesting
D-11 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1187 HARRIGAN 200245 Design: Consecutive patients 

Sample Size: 6275 Year/Range: NR 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Africa 

Med Class: Non-NRTI, NRTI Inclusions: Antiretroviral naïve, Available information on ARV regimens 

SelectioTestingbased VIRCO

2043 JACK 200446 Design: Consecutive patients 

Sample Size: 20 Year/Range: 2002 

Population: Adults (NOS), Not Tx naïve Age/Range: 31 / 18-53 Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Age ≥ 18 years, and Pulmonary TB 

SelectioTreatmTestingbased 

2042 JEANNIN 200447 Design: Case series, sample assembly NR 

Sample Size: 398 Year/Range: 2004 

Population: Adults (NOS), Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: ARV treatment ≥ 6 mo 

SelectioTreatmTesting

1453 JENWITHEESUK 200348 Design: Case series, sample assembly NR 

Sample Size: 171 Year/Range: 2001-2002 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: Other Asia 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Viral load > 500 HIV RNA copies/ml, ARV experienced 

SelectioTestingbased 

1473 JOHANN-LIANG 200049 Design: Consecutive patients 

Sample Size: 40 Year/Range: NR 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Not Tx naïve Age/Range: NR / 1-14 Region: US/Canada 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Viral load > 1000 copies/ml and Currently on ARV Tx 

SelectioTestingbased 
D-12 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1007 JOHNSON 200550 Design: Clinical trial 

Sample Size: 50 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: 32 - 38 weeks gestation 

SelectioTestingbased 

1034 JOURDAIN 200451 Design: Clinical trial and other method 

Sample Size: 269 Year/Range: 2001-2003 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Other Asia 

Med Class: Non-NRTI Inclusions: > 28 weeks gestation and CD4 cell count < 250/ml2 

SelectioTestingbased 

JOURDAIN 200452

Design: Clinical trial Sample Size: 219 Year/Range: NR 

Population: Pregnant women, Not TX naive Age/Range: NR / NR Region: Other Asia 

Med Class: Non-NRTI Inclusions: Received pMTCT, Initiated NNRTI based-regimen 

SelectioTestingbased 

1221 KAMKAMIDZE 200153 Design: Random sample of larger database 

Sample Size: 49 Year/Range: 1992-1999 

Population: Children (under 12 yrs), Tx naïve Age/Range: NR / 0-16 Region: US/Canada 

Med Class: NRTI Inclusions: NR 

SelectioTestingPCR 

1613 KANTOR 200254 Design: Case series, sample assembly NR 

Sample Size: 21 Year/Range: 2001 

Population: Adults (NOS), Tx naïve Age/Range: NR / 31-61 Region: Africa 

Med Class: NRTI, Protease inhibitor Inclusions: On current ARV for ≥ 2 months 

SelectioTestingbased 
D-13 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

2085 KANTOR 200355 Design: Case series, sample assembly NR 

Sample Size: 34 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: NR 

SelectioTestingbased 

1991 KANTOR 200556 Design: Cohort, sample assembly NR 

Sample Size: 379 Year/Range: NR 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Latin America, Africa, Japan, Other Asia 

Med Class: Non-NRTI, NRTI Inclusions: Failing first line regimen 

SelectioTesting

1777 KARCHAVA 200657 Design: Case series, sample assembly NR 

Sample Size: 42 Year/Range: 2001-2002 

Population: Children (under 12 yrs), Not Tx naïve Age/Range: NR / NR Region: US/Canada 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: NR 

SelectioTestingbased 

2050 KARCHER 200458 Design: Case series, sample assembly NR 

Sample Size: 76 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, adults (NOS), Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: NR 

SelectioTesting

1675 KIJAK 200159 Design: Clinical trial and random sample of larger 

database Sample Size: 107 Year/Range: 1997-2000 

Population: IV drug users, and adults (NOS), Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased based s
D-14 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1487 KINOMOTO 200560 Design: Case series, sample assembly NR 

Sample Size: 39 Year/Range: 2001-2002 

Population: Adults (NOS), Tx naïve Age/Range: NR / 30-40 Region: Africa 

Med Class: Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased assay 

1676 KONINGS 200461 Design: Random sample of larger database 

Sample Size: 128 Year/Range: 2000-2002 

Population: Adolescents (12-18 yrs), women, Tx naïve Age/Range: 35 / 17-70 Region: Africa 

Med Class: Protease inhibitor Inclusions: Tx naïve 

SelectioTestingbased 

1984 LAMA 200562 Design: Consecutive patients 

Sample Size: 375 Year/Range: 2002-2003 

Population: Men who have sex with men, and adults (NOS), Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Male who had sex with a man in past year 

SelectioTestingbased 

1679 LAN 200363 Design: Case series, sample assembly NR 

Sample Size: 200 Year/Range: 2001-2002 

Population: IV drug users, adolescents (12-18 yrs), and adults (NOS), Tx naïve Age/Range: NR / 15-52 Region: Other Asia 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 

1127 LARBALESTIER 200364 Design: Cohort, sample assembly NR 

Sample Size: 91 Year/Range: 1996-2001 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Western Europe 

Med Class: NRTI Inclusions: NR 

SelectioTestingbased based s
D-15 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

2092 LAURENT 200265 Design: Case series, sample assembly NR 

Sample Size: 58 Year/Range: 1998-2000 

Population: Adults (NOS), Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: NRTI, Protease inhibitor Inclusions: Tx naïve, High risk of AIDS progression 

SelectioTreatmTestingbased 

2015 LAURENT 200466 Design: Clinical trial 

Sample Size: 60 Year/Range: 2002-2003 

Population: Adults (NOS), Not Tx naïve Age/Range: 35 / 29-41 Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: HIV-1 group M infection, and Age ≥

18 years, and AIDS diagnosis, and Hemoglobin ≥ 8 g/dL, and Antiretroviral naïve 

SelectioTestingbased 

2017 LAURENT 200567 Design: Consecutive patients 

Sample Size: 176 Year/Range: 1998-2001 

Population: Adults (NOS), Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Age > 15 

SelectioTreatmTestingbased 

LEE 200568

Design: Clinical trial Sample Size: 32 Year/Range: NR/2000-2001 

Population: Pregnant women, Not TX naive Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Received pMTCT 

SelectioTestingbased 

1957 LEHMAN 200569 Design: Clinical trial 

Sample Size: 30 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: NR 

SelectioTestingspecific 
D-16 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

LOUBSER 200670

Design: Consecutive patients Sample Size: 67 Year/Range: NR 

Population: Pregnant women, Not TX naive Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Received pMTCT, ARV naïve prior to pregnancy 

SelectioTestingspecific 

LOUBSER 200571

Design: Case series, sample assembly NR Sample Size: NR Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Received pMTCT 

SelectioTestingtime PC

1936 LOUBSER 200472 Design: Case series, sample assembly NR 

Sample Size: NR Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Received pMTCT 

SelectioTestingbased 

1686 LY 200573 Design: Consecutive patients 

Sample Size: 146 Year/Range: 2003-2004 

Population: Pregnant women, and adults (NOS), Tx naïve Age/Range: NR / NR Region: Asia 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, Tested HIV+ in the last year 

SelectioTestingbased 

1022 LYONS 200574 Design: Cohort, sample assembly NR 

Sample Size: 39 Year/Range: NR 

Population: Pregnant women, and adults (NOS), Not Tx naïve Age/Range: NR / 16-32 Region: Western Europe 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: > 28 weeks gestation, CD4 cell count > 300 x 106/l 

SelectioTestingbased 
D-17 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1687 MACHADO 200475 Design: Consecutive patients 

Sample Size: 75 Year/Range: 1999-2002 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Not Tx naïve Age/Range: 7 / 1-14 Region: Latin America 

Med Class: NRTI, Protease inhibitor Inclusions: Age ≤ 14 years, ARV Tx for at least 3 months 

SelectioTestingbased 

2008 MARCELIN 200676 Design: Case series, sample assembly NR 

Sample Size: 109 Year/Range: 2004-2005 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: NR 

SelectioTesting

MARTINSON 200677

Design: Consecutive patients Sample Size: 53 Year/Range: NR/2002-2003 

Population: Children (under 12 yrs), Not TX naive Age/Range: 1 / NR Region: Africa 

Med Class: Non-NRTI Inclusions: > 32 weeks gestation 

SelectioTestingbased 

2061 MARTINSON 200478 Design: Case series, sample assembly NR 

Sample Size: NR Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Infected during birth, Received pMTCT 

SelectioTesting

1911 MATHUR 200579 Design: Consecutive patients 

Sample Size: 49 Year/Range: 2000 

Population: Children (under 12 yrs), Not Tx naïve Age/Range: NR / NR Region: US/Canada 

Med Class: Protease inhibitor Inclusions: NR 

SelectioTesting
D-18 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1955 MCINTYRE 200580 Design: Clinical trial 

Sample Size: 454 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: NR 

SelectioInfected Testingbased 

1948 MILLER 200481 Design: Clinical trial 

Sample Size: 600 Year/Range: NR 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Latin America 

Med Class: Non-NRTI, NRTI Inclusions: Antiretroviral naïve 

SelectioTreatmTesting

1605 MOFENSON 200082 Design: Clinical trial 

Sample Size: 74 Year/Range: 1993-1997 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: US/Canada 

Med Class: NRTI, Protease inhibitor Inclusions: Received ZDV Tx during pregnancy, CD4 < 350 

SelectioTestingbased 

1052 MORRIS 200383 Design: Case series, sample assembly NR 

Sample Size: 163 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Clade C 

SelectioTreatmTestingbased 

2062 MORRIS 200484 Design: Cohort, sample assembly NR 

Sample Size: 175 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Infected during birth, Received pMTCT 

SelectioTestingbased 
D-19 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1062 MULLEN 200285 Design: Case series, sample assembly NR 

Sample Size: 26 Year/Range: 1996-2000 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Not Tx naïve Age/Range: NR / 0-15 Region: Western Europe 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: NR 

SelectioTestingbased 

1902 NGO-GIANG- HUONG 

200586

Design: Clinical trial Sample Size: 50 Year/Range: NR 

Population: Children (under 12 yrs), Not Tx naïve Age/Range: NR / NR Region: Asia 

Med Class: Non-NRTI, NRTI Inclusions: Received pMTCT 

SelectioTestingbased 

1910 NURUTDINOVA 200587 Design: Cohort, sample assembly NR 

Sample Size: 80 Year/Range: 1999-2004 

Population: Pregnant women, Tx naïve Age/Range: 37 / NR Region: US/Canada 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: NR 

SelectioTesting

PALMER 200688

Design: Consecutive patients Sample Size: 22 Year/Range: NR 

Population: Pregnant women, Not TX naive Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Received pMTCT 

SelectioTestingbased RT-PC

1956 PALMER 200589 Design: Clinical trial 

Sample Size: 32 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI Inclusions: NR 

SelectioTestingspecific 
D-20 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1204 PALUMBO 200190 Design: Clinical trial 

Sample Size: 244 Year/Range: 1991-1997 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: US/Canada 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Viral load > 1000 copies/ml and Recorded AZT duration during pregnancy 

SelectioTestingbased 

1125 PARK 200391 Design: Case series, sample assembly NR 

Sample Size: 50 Year/Range: 1998-2002 

Population: IV drug users, and men who have sex with men, and adults (NOS), Tx naïve Age/Range: 40 / 22-71 Region: Other Asia 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, Virus level > 3.0 log10 copies/ml 

SelectioTestingbased 

1700 PEREZ 200192 Design: Clinical trial 

Sample Size: 26 Year/Range: 1996-1999 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Tx naïve Age/Range: NR / 1-17 Region: US/Canada 

Med Class: NRTI, Protease inhibitor Inclusions: Protease Inhibitor naïve, and Viral load > log10 copies/mL 

SelectioTestingbased 

1778 PEREZ 200693 Design: Clinical trial 

Sample Size: 20 Year/Range: NR 

Population: Pregnant women, Not Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI Inclusions: Started ZDV/3TC/NVP in 2nd or 3rd trimester, ARV naïve prior to pregnancy 

SelectioTestingbased 
D-21 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1703 PETCH 200594 Design: Case series, sample assembly NR 

Sample Size: 21 Year/Range: 1996-2001 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Tx naïve 

SelectioTestingbased 

1704 PIENIAZEK 200495 Design: Case series, sample assembly NR 

Sample Size: 76 Year/Range: 1986-1999 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Latin America, Africa 

Med Class: Protease inhibitor Inclusions: Tx naïve, HIV-2 infection 

SelectioTestingPCR 

1706 PILLAY 200296 Design: Clinical trial 

Sample Size: 37 Year/Range: 2000 

Population: Pregnant women, Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Antiretroviral naïve 

SelectioTestingPCR 

1707 PIRES 200497 Design: Case series, sample assembly NR 

Sample Size: 56 Year/Range: 2000-2002 

Population: Men who have sex with men, women, Tx naïve Age/Range: 28 / NR Region: Latin America 

Med Class: NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 
D-22 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1823 PUTHANAKIT 200598 Design: Cohort, sample assembly NR 

Sample Size: 96 Year/Range: 2000-2003 

Population: Children (under 12 yrs), adolescents (12-18 yrs), Not Tx naïve Age/Range: 8 / 2-14 Region: Asia 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, CD4 % < 15% 

SelectioTesting

1711 RICHARD 200499 Design: Cohort, sample assembly NR 

Sample Size: 86 Year/Range: 1996-2002 

Population: Adults (NOS), Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: NR 

SelectioTestingbased Virolog

1020 RODRIGUES 2005100 Design: Consecutive patients 

Sample Size: 306 Year/Range: 2001-2003 

Population: Children (under 12 yrs), adolescents (12-18 yrs), and pregnant women, Not Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Available information on ARV regimens, Clinical indication for genotype testing 

SelectioTestingbased 

1718 SAAG 2004101 Design: Clinical trial 

Sample Size: 580 Year/Range: 2000-2002 

Population: Adults (NOS), Tx naïve Age/Range: 36 / 18-69 Region: US/Canada, Western Europe, Latin America and 

Med Class: Non-NRTI, NRTI Inclusions: Age ≥ 18 years, Viral load > 5,000 copies RNA/ml 

SelectioTestingPCR 
D-23 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1395 SACHDEVA 2005102 Design: Consecutive patients 

Sample Size: 60 Year/Range: 2000-2002 

Population: Children and adults (NOS), Tx naïve Age/Range: 31 / 1-67 Region: India 

Med Class: NRTI Inclusions: Antiretroviral naïve 

SelectioTestingPCR 

1833 SCHAPIRO 2005103 Design: Clinical trial 

Sample Size: 1483 Year/Range: NR 

Population: Population NR, Not Tx naïve Age/Range: NR / NR Region: US/Canada, Western Europe, Australia/NZ, Latin America 

Med Class: Protease inhibitor Inclusions: ARV Tx with nucleosides, or nonnucleosides, or PIs, or Prior exposure to unboosted SQV regimen 

SelectioTestingbased phenot

SHAPIRO 2006104 Design: Clinical trial 

Sample Size: 709 Year/Range: NR/2002-2003 

Population: Pregnant women, Not TX naive Age/Range: NR / 18-99 Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Age >= 18 years, Hemoglobin >= 8 g/dL, 32 - 35 weeks gestation, Absolute neutrophil count >=1.0 X 109/L, Infant with known HIV status 

SelectioTestingbased 

1224 SITNITSKAYA 2001105 Design: Cohort, sample assembly NR 

Sample Size: 64 Year/Range: 1995-1999 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: US/Canada 

Med Class: NRTI Inclusions: Viral load > 1000 copies/ml, Infant with known HIV status 

SelectioTestingbased based s
D-24 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

SPACEK 2006106 Design: Consecutive patients 

Sample Size: 137 Year/Range: 2003/NR-NR 

Population: Women, Not TX naive Age/Range: 39 / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Continuous ARV >= 12 weeks 

Selectioload levTestingbased assay 

1411 SUTTHENT 2005107 Design: Cohort, sample assembly NR 

Sample Size: 542 Year/Range: 1998-2003 

Population: Children (under 12 yrs), pregnant women, and adults (NOS), Not Tx naïve Age/Range: NR / NR Region: Asia 

Med Class: Non-NRTI, NRTI Inclusions: NR 

SelectioTestingbased 

1231 TANURI 1999108 Design: Convenience sample 

Sample Size: 76 Year/Range: 1993-1997 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: Latin America 

Med Class: Protease inhibitor Inclusions: PI naïve 

SelectioTestingbased assay 

TONI 2005109 Design: Case series, sample assembly NR 

Sample Size: 29 Year/Range: NR 

Population:Pregnant women, Not TX naive Age/Range: 30 / NR Region: Africa 

Med Class: Non-NRTI Inclusions: Received pMTCT 

SelectioTestingbased 
D-25 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1731 TONI 2003110 Design: Case series, sample assembly NR 

Sample Size: 107 Year/Range: 2001-2002 

Population: Pregnant women and adults (NOS), Tx naïve Age/Range: 28 / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, and Seroconversion within 3 years 

SelectioTestingbased 

1074 TONI 2002111 Design: Consecutive patients 

Sample Size: 99 Year/Range: 1997-2000 

Population: Adults (NOS), Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, and Seroconversion within 3 years 

SelectioTestingbased assay 

1959 TROYER 2005112 Design: Cohort, sample assembly NR 

Sample Size: 398 Year/Range: NR 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI Inclusions: Received pMTCT 

SelectioTestinglabeled (OLA) 

1738 VERGNE 2000113 Design: Case series, sample assembly NR 

Sample Size: 142 Year/Range: 1995-1999 

Population: Population NR, Tx naïve Age/Range: NR / NR Region: Western Europe, Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve 

SelectioTestingbased 
D-26 

HIDE 

ID 

First author Year Reference # 

Study Design Sample Size Year/Range Data Collected 

Population Age/Age Range Region 

Medication Class Inclusion Criteria 

SelectioResista

1087 VERGNE 2003114 Design: Case series, sample assembly NR 

Sample Size: 80 Year/Range:1998-2001 

Population: Adults (NOS), Not Tx naïve Age/Range: NR / NR Region: Africa 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: AIDS diagnosis, and High risk of AIDS progression 

SelectioTreatmTestingbased 

1375 WALMSLEY 2002115 Design: Clinical trial 

Sample Size: 686 Year/Range: 1999 

Population: Adolescents (12-18 yrs), and adults (NOS), Not Tx naïve Age/Range: 38 / 19-84 Region: US/Canada, Western Europe, Australia/NZ, Latin America, Africa 

Med Class: Protease inhibitor Inclusions: Plasma RNA > 400 copies/ml 

SelectioNelfinaD30N aTestingbased Virolog

1275 WELLES 2000116 Design: Convenience sample 

Sample Size: 142 Year/Range: 1989-1994 

Population: Children (under 12 yrs), pregnant women, Not Tx naïve Age/Range: NR / 24-32 Region: US/Canada, Latin America 

Med Class: NRTI Inclusions: Received ZDV Tx during pregnancy 

SelectioTestingbased 

1413 ZHANG 2004117 Design: Case series, sample assembly NR 

Sample Size: 53 Year/Range: NR 

Population: IV drug users, Tx naïve Age/Range: 40 / 14-60 Region: Asia 

Med Class: Non-NRTI, NRTI, Protease inhibitor Inclusions: Antiretroviral naïve, AIDS diagnosis 

SelectioTestingPCR, R
D-27 

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 50. Johnson JA, Li JF, Morris L et al. Emergence of 

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 51. Jourdain G, Ngo-Giang-Huong N, Le Coeur S et 

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 52. Jourdain G, Ngo-Giang-Huong N, Tungyai P et 

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Appendix E: Rejected Titles 

E-1 

Reject: At Abstract 

 1. Continuously effective and well tolerated primary 

HIV therapy: Lopinavir/r - No resistance after 5 

years Original>Anhaltend Wirksame Und 

Vertragliche Hiv-Ersttherapie: Auch Nach Funf 

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Dec; 145(50):60-61. 

Rec #: 1419 

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Infections in Medicine. 2002; 19(2):50. 

Rec #: 1403 

 3. HIV cross-resistance to saquinavir is less frequent, 

slower to develop than other proteinase inhibitors. 

Formulary. 1995; ISSN: 0098-6909. 

Rec #: 1508 

 4. HIV drug resistance is on the increase. 

Pharmaceutical Journal. 2003 Nov; 271(7273):604. 

Rec #: 1426 

 5. HIV resistance to kaletra seen to be very rare. Clin 

Infect Dis. 2004 Aug; 39(4):iv. 

Rec #: 1429 

 6. Justified hope after four years: First antiretroviral 

therapy still without resistance 

Original>Berechtigte Hoffnung Nach Vier Jahren: 

Ersttherapie Immer Noch Ohne Resistenzen. 

MMW-Fortschr Med. 2003; 145(SUPPL. 1):48-49. 

Rec #: 1430 

 7. Zidovudine resistance among HIV infected 

children: Association with advanced disease. 

Canadian Journal of Infectious Diseases. 2001; 

12(2):113-114. 

Rec #: 1414 

 8. Bacheler, L. T.; Anton, E. D.; Kudish, P., and et al. 

Impact of baseline NNRTI Resistance on the 

efficacy of efavirenz combination therapy in 

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Prevalence of mutations associated with 

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Rec #: 2099 

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emergence of resistance in a blinded phase III study 

with kaletra (lopinavir/ritonavir) or nelfinavir plus 

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Interscience Conference on Antimicrobial Agents 

and Chemotherapy; Chicago. 2001. 

Rec #: 1537 

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Ziekenhuis Utrecht, Heidelberglaan 100, 3584 CX 

Utrecht. Netherlands). The value of HIV resistance 

determination for the hospital: Not all resistances 

are alike: <ORIGINAL> De waarde van HIVresistentiebepalingen voor de kliniek: de ene 

resistentie is de andere niet. Pharmaceutisch 

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heavily treated patient s referred to a reference lab 

in the UK. 1999. 

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Original>Resistance Du Vih Aux Inhibiteurs De 

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DEC.):S19-S28. 

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response to therapy: final analysis of a randomised 

trial (VIRA3001). Antivir Ther. 2000; 5:67-8. 

Rec #: 1575 
E-2 

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Identification of amino acid substituions correlated 

with reduced atazanavir susceptibility in patients 

treated with atazanavir-containing regimens 

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Rec #: 1587 

 19. Dalmau, D.; Ochoa de Echaguen, A.; Martinez, E., 

and et al. NEFA simplification trial: patterns of 

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 20. De, Clercq E. (E. De Clercq, Rega Institute Medical 

Research, Katholieke Universiteit, 

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Belgium). Development of resistance of human 

immunodeficiency virus (HIV) to anti-HIV agents: 

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Wolf, F., and Goudsmit, J. [Zidovudine-resistant 

HIV strains in untreated intravenous drug users and 

homosexual men in Amsterdam infected in 1996]. 

Ned Tijdschr Geneeskd. 1997 Oct 18; 

141(42):2030-1. 

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 22. De Meyer, S. ; Van Marck, H.; Van De Bulcke, T.; 

Vingerhoets, J.; Azin, H.; Pauwels, R., and et al. 

Phenotypic and genotypic profiling of TMC 114 a 

potent next-generation PI, against some 1600 recent 

PI-resistant clinical isolates. 11th Conference On 

Retroviruses And Opportunistic Infections; San 

Francisco. 2004. 

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 23. De Meyer, S. ; Van Marck, H.; Veldeman, J.; 

McKenna, P.; Pauwels, R., and Bethune, M. P. 

Antiviral Activity of TMC114 , a potent nextgenreation PI, against > 4000 recent recombinant 

clinical isolates exhibiting a wide range of (PI) 

resitance profiles. 12th International HIV Drug 

Resistance Workshop; Cabo San Lucas, Mexico. 

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Rec #: 1567 

 24. Funk, M. B.; Linde, R.; Wintergerst, U.; Schuster, 

T.; Notheis, G.; Sturmer, M.; Kurowski, M.; 

Klingebiel, T., and Kreuz, W. Benefit, resistance 

and compliance in HIV-infected children on an 

inital antiretroviral triple therapy for a period of two 

years Original>Wirksamkeit, Resistenzentwicklung 

Und Compliance Bei Hiv-Infizierten Kindern Unter 

Einer 2-Jahrigen, Primaren Antiretroviralen 3fachTherapie. Monatsschrift Fur Kinderheilkunde. 2002; 

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 25. Grandadam, M.; Nicand, E.; Koeck, J. L.; Caron, 

M., and Teyssou, R. Resistance of African human 

immunodeficiency virus to active antiretroviral 

treatment: Need for virological surveillance 

Original>Etat De La Resistance Des Souches De 

Vih-1 En Afrique: Quelle Place Pour Les Reseaux 

De Surveillance Virologique. Medecine Tropicale. 

2002; 62(1):89-93. 

Rec #: 1435 

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Rec #: 1569 

 27. Haubrich, R. ; Hellmann, N.; Keiser, P., and et al. 

The clinical relevance of non-nucleoside reverse 

transcriptase inhibitor hypersusceptibility: a 

prospective cohort analysis [abstract ThOrB1388]. 

XIV International AIDS Conference; Barcelona. 

Barcelona: Prous Science, S.A.; 2002: 377. 

Rec #: 1584 

 28. Haubrich, R. ; Keiser, P.; Lie, Y. S.; Leedom, J.; 

Richman, D.; McCutchan, J. A., and et al. CCTG 

575: A randomized, prospective study of phenotype 

testing versus standard of care for patients failing 

antiretroviral therapy [Abstract 80]. Antivir Ther. 

2001; 6(Supl. 1):63-71. 

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 29. Hofmann-Assmus, M. Long-term HIV therapy 

without resistance development Original>Hiv: 

Langzeitwirkung Ohne Resistenzbildung. 

Pharmazeutische Zeitung. 2004 Dec; 149(50):40. 

Rec #: 1431 

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Lack of multidrug resistance in nonresponders to 

antiretroviral therapy with poor adherence. 1st 

International AIDS Society Conference on HIV 

Pathogenesis and Treatment; Buenos Aires. 

International AIDS Society, Stockholm, Sweden; 

2002. 

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 31. Hsu, A.; Kempf, D.; Granneman, R., and et al. 

Exploring theorical mechanisms for lack of 

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naive subjects [abstract 436-W]. 9th Conference on 

Retroviruses and Opportunistic 

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Rec #: 1586 
E-3 

 32. Kemp, S. D.; Salim, M.; Stammers, D., and et al. A 

mutation in HIV-1 reverse transcriptase at codon 

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reverse transcriptase inhibitor resistance in clinical 

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Rec #: 1571 

 33. King, M.; Brun, S.; Tschampes, J., and et al. 

Exploring the effects of adherence on resistance: 

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Original>Kombinierte Proteasehemmer Gegen 

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M184V mutation. Antivir Ther. 2003 Feb; 8(1):51-

6. 

Rec #: 1165 

 161. Zaccarelli, M.; Perno, C. F.; Forbici, F.; Soldani, F.; 

Bonfigli, S.; Gori, C.; Trotta, M. P.; Bellocchi, M. 

C.; Liuzzi, G.; D'Arrigo, R.; De Longis, P.; Boumis, 

E.; Bellagamba, R.; Tozzi, V.; Narciso, P., and 

Antinori, A. Q151M-mediated multinucleoside 

resistance: prevalence, risk factors, and response to 

salvage therapy. Clin Infect Dis. 2004 Feb 1; 

38(3):433-7. 

Rec #: 1117 
E-76 

Rejected : Second screening - No prevalence or incidence 

data 

 1. Antinori, A.; Trotta, M.; Lorenzini, P.; Carosi, G.; 

Gianotti, N.; Maggiolo, F.; Torti, C.; Castagna, A.; 

Andreoni, M., and Perno, C. F. Virological 

Response to ART in the Presence of K65R 

Mutation [Impact of Resistance on Treatment 

Response]. 13th Conference on Retroviruses and 

Opportunistic Infections; 2006. 

Rec #: 1812 

 2. Baxter, J. D. ; Leduc, R. E.; DuChene, A.; Leong, 

H.; Furtado, M. R., and Petrauskene, O. V. 

Prevalence of HIV-1 GAG cleavage site mutations 

in patients failing protease inhiitors in the GART 

Study (CPCRA 046). 2004; 9, S48. 

Rec #: 1913 

 3. Baxter JD; Mayers DL; Wentworth DN; Neaton JD; 

Hoover ML; Winters MA; Mannheimer SB; 

Thompson MA; Abrams DI; Brizz BJ; Ioannidis JP, 

and Merigan TC (Cooper Hospital/UMDNJ-Robert 

Wood Johnson Medical School, Camden, NJ, 

USA.). A randomized study of antiretroviral 

management based on plasma genotypic 

antiretroviral resistance testing in patients failing 

therapy. CPCRA 046 Study Team for the Terry 

Beirn Community Programs for Clinical Research 

on AIDS. AIDS. 2000 Jun; 14(9):F83-93. 

Rec #: 1383 

 4. Cingolani, A.; Antinori, A.; Rizzo, M. G.; Murri, 

R.; Ammassari, A.; Baldini, F.; Di Giambenedetto, 

S.; Cauda, R., and De Luca, A. Usefulness of 

monitoring HIV drug resistance and adherence in 

individuals failing highly active antiretroviral 

therapy: a randomized study (ARGENTA). AIDS. 

2002 Feb 15; 16(3):369-79. 

Rec #: 1549 

 5. Cohen, C. J.; Hunt, S.; Sension, M.; Farthing, C.; 

Conant, M.; Jacobson, S.; Nadler, J.; Verbiest, W.; 

Hertogs, K.; Ames, M.; Rinehart, A. R., and 

Graham, N. M. A randomized trial assessing the 

impact of phenotypic resistance testing on 

antiretroviral therapy. AIDS. 2002 Mar 8; 

16(4):579-88. 

Rec #: 1547 

 6. Costagliola, D.; Morand-Joubert, L.; Assoumou, L.; 

Brodard, V.; Plantier, J. C.; Delaugerre, C.; 

Mackiewicz, V.; Saidi, S.; Brun-Vezinet, F.; 

Masquelier, B., and ANRS AC11 Resistance Study 

Group. Prevalence of Resistance to at Least 1 Drug 

in Treated-HIV-infected Patients with Viral Load 

>1000 Copies/mL in 2004: A French Nationwide 

Study [Epidemiology and Transmission of 

Resistance]. 13th Conference on Retroviruses and 

Opportunisitic Infections; 2006. 

Rec #: 1775 

 7. Durant, J.; Clevenbergh, P.; Halfon, P.; Delgiudice, 

P.; Porsin, S.; Simonet, P.; Montagne, N.; Boucher, 

C. A.; Schapiro, J. M., and Dellamonica, P. Drugresistance genotyping in HIV-1 therapy: the 

VIRADAPT randomised controlled trial. Lancet. 

1999 Jun 26; 353(9171):2195-9. 

Rec #: 1546 

 8. Duvivier, C.; Ghosn, J.; Wirden, M.; Ouagari, Z.; 

Dominguez, S.; Marcelin A.G.; Peytavin, G., and 

Katlama, C. Efficacy and Safety of Dual Boosted PI 

Regimen without RT Inhibitors in HIV-1-infected 

Patients. 12th Conference on Retroviruses and 

Opportunistic Infections; 2005. 

Rec #: 1871 

 9. El-Far, F. Medeiros E. A. S. Gasparoto C. T. Diaz 

R. S. (Dr. R.S. Diaz, Laboratorio de Retrovirologia, 

Infectious Disease Division, Federal University of 

Sao Paulo). Antiretroviral drug resistance among 

patients with human immunodeficiency virus who 

act as sources or potential sources in occupational 

accidents involving healthcare workers. Infect 

Control Hosp Epidemiol . 2005 Sep; 26(9):782-8; 

ISSN: 0899-823X. 

Rec #: 1499 

 10. Gunthard, H. ; von Wyl, V.; Yerly, S.; Boni, J.; 

Schupbach, J.; Burgisser, P.; Klimkait, T.; Battegay, 

M.; Furrer, H.; Telenti, A.; Hirschel, B.; Vernazza, 

P.; Bernasconi, E.; Rickenbach, M.; Perrin, L., and 

Ledergerber, B. Virologicdal failure and emergence 

of treatment-specific HIV-1 drug resistance patterns 

on first-line HAART in previously untreated 

patients from the Swiss HIV Cohort Study (SHCS). 

Antivir Ther. 2006; 11:S82. 

Rec #: 2005 
E-77 

 11. Haubrich, R. ; Hernandez, J.; Bates, M.; Thompson, 

M.; Margolis, D.; Pappa, K.; Yau, L., and Schooley, 

R. Determinants of replication capacity (RC) in 

HIV-1 isolates from antiretroviral (ART)-

experienced adults failing a PI-based regimen, and 

relationship of RC with HIV-1 RNA and CD4 

counts. 2004; 9, S162. 

Rec #: 1941 

 12. Hertogs, K.; Bloor, S.; Kemp, S. D.; Van den 

Eynde, C.; Alcorn, T. M.; Pauwels, R.; Van Houtte, 

M.; Staszewski, S.; Miller, V., and Larder, B. A. 

Phenotypic and genotypic analysis of clinical HIV-1 

isolates reveals extensive protease inhibitor crossresistance: a survey of over 6000 samples. AIDS. 

2000 Jun 16; 14(9):1203-10. 

Rec #: 1215 

 13. Marcelin, A. G.; Roquebert, B.; Malet, I.; Wirden, 

M.; Katlama, C., and Calvez, V. Minor protease 

inhibitor resistant variants, even at very low level, 

can drive the failure resistance mutations profiles of 

subsequent protease inhibitor-based regimen. 2004; 

9, S164. 

Rec #: 1943 

 14. Masquelier, B.; Race, E.; Tamalet, C.; Descamps, 

D.; Izopet, J.; Buffet-Janvresse, C.; Ruffault, A.; 

Mohammed, A. S.; Cottalorda, J.; Schmuck, A.; 

Calvez, V.; Dam, E.; Fleury, H., and Brun-Vezinet, 

F. Genotypic and phenotypic resistance patterns of 

human immunodeficiency virus type 1 variants with 

insertions or deletions in the reverse transcriptase 

(RT): multicenter study of patients treated with RT 

inhibitors. Antimicrob Agents Chemother. 2001 

Jun; 45(6):1836-42. 

Rec #: 1232 

 15. Mougnutou, R.; Bourgeois, A.; Nkoue, N.; Laurent, 

C.; Lactouock, B.; Liegeois, F., and et al. 

Evaluation of a AART pilot study in Yaounde, 

Cameroon: 24 months follow-up. 2nd AIS 

Conference on HIV Pathogenesis and Treament; 

Paris. 2003. 

Rec #: 2046 

 16. Phillips, A. N.; Dunn, D.; Sabin, C., and et al. Risk 

of development of drug resistance in patients 

starting antiretroviral therapy with three or more 

drugs in routine clinical practice. 2004; 9, S151. 

Rec #: 1938 

 17. Quiros-Roldan, E.; Signorini, S.; Castelli, F.; Torti, 

C.; Patroni, A.; Airoldi, M., and Carosi, G. Analysis 

of HIV-1 mutation patterns in patients failing 

antiretroviral therapy. J Clin Lab Anal. 2001; 

15(1):43-6. 

Rec #: 1197 

 18. Race, E.; Dam, E.; Obry, V.; Paulous, S., and 

Clavel, F. Analysis of HIV cross-resistance to 

protease inhibitors using a rapid single-cycle 

recombinant virus assay for patients failing on 

combination therapies. AIDS. 1999 Oct 22; 

13(15):2061-8. 

Rec #: 1227 

 19. Riddler, S.; Jiang, H.; Deeks, S.; Tenorio, A.; 

Huang, H.; Kuritzkes, D.; Acosta, E.; Landay, A.; 

Bartlett, J., and Aids Clin Trials Group. A 

Randomized Pilot Study of Delayed ART Switch in 

Subjects with Detectable Viremia on HAART 

[Antiretroviral Therapy: Randomized Trials, 

Strategies and Long-Term Outcomes]. 13th 

Conference on Retroviruses and Opportunistic 

Infections; 2006. 

Rec #: 1807 

 20. Rodrigues, R.; Custodio, R. M.; Bueno, S. M.; Eira, 

M.; Ferreira, J. L.; Jamal, L.; Duarte, A. J., and 

Brigido, L. F. Prevalence of ARV resistance 

mutations and impact of genotyping test in HIV 

patients with advance disease in Sao Paulo, Brazil. J 

Clin Virol. 2005 Apr; 32(4):336-7. 

Rec #: 1452 

 21. Schmidt, B.; Korn, K.; Moschik, B.; Paatz, C.; 

Uberla, K., and Walter, H. Low level of crossresistance to amprenavir (141W94) in samples from 

patients pretreated with other protease inhibitors. 

Antimicrob Agents Chemother. 2000 Nov; 

44(11):3213-6. 

Rec #: 1205 

 22. Schnell, T.; Schmidt, B.; Moschik, G.; Thein, C.; 

Paatz, C.; Korn, K., and Walter, H. Distinct crossresistance profiles of the new protease inhibitors 

amprenavir, lopinavir, and atazanavir in a panel of 

clinical samples. AIDS. 2003 May 23; 17(8):1258-

61. 

Rec #: 1109 

 23. Shulman, N. S.; Bosch, R. J.; Albrecht, M.; 

Hellmann, N.; Katzenstein, D. A., and ACTG 365 

team. Impact of the M184V/I on protease inhibitor 

susceptibilities in protease inhibitor-naive patients. 

2004; 9, S84. 

Rec #: 1919 

 24. Smith, A. J. ; Wang, H.; Bennett, D.; Teshale, E.; 

Buskin, S.; Morse, A.; Wohl, A.; Swerdlow, D.; 

Sullivan, P., and Wolfe, M. Prevalence of mutations 

associated with antiretroviral drug resistance 

(ARVDR) in a cohort of treated individuals in four 

US cities. 2004; 9, S112. 

Rec #: 1933 
E-78 

 25. Spacek, L. A.; Shihab, H. M.; Mwesigire, D.; 

Ronald, A.; Kamya, M.; Mayanja, H.; Moore, R. D., 

and Quinn, T. C. Drug resistance in patients iwth 

HIV-1 non-B subypes in Kampala, Uganda. 42nd 

Annual Meeting of IDSA; Boston, MS. 2004. 

Rec #: 2090 

 26. Sugiura, W.; Matsuda, M.; Chiba, T., and et al. 

Changes in prevalence and patterns of drug resistant 

mutations in Japan - summary of nationwide HIV-1 

drug resistance surveillance study (1996 to 2003) in 

Japan. 2004; 9, S109. 

Rec #: 1930 

 27. Swartz, E. C.; Defore, K. T.; Horvath, J. A.; Postic, 

B., and Talwani, R. Differences in virologic, 

immunologic, and genotypic responses according to 

regimen class during time on first HAART regimen 

started in treatment naive HIV-infected patients 

(pts) treated at a publicly funded clinic. 42nd 

Annual Meeting of IDSA; Boston, MS. 2004. 

Rec #: 2086 

 28. Torti, C.; Quiros-Roldan E. ; Regazzi M. ; De Luca 

A. ; Mazzotta F. ; AntinoriA. ; Ladisa N. ; Micheli 

V. ; Orani A. ; Patroni A. ; Villani P. ; Lo CaputoS. 

; Moretti F. ; Di Giambenedetto S. ; Castelnuovo F. 

; Maggi P. ; TinelliC. , and Carosi G. (Dr. C. Torti, 

Institute for Infectious and Tropical Diseases). A 

randomized controlled trial to evaluate antiretroviral 

salvage therapy guided by rules-based or 

phenotype-driven HIV-1 genotypic drug-resistance 

interpretation with or without concentrationcontrolled intervention: The resistance and dosage 

adapted regimens (RADAR) study. Clin Infect Dis. 

2005 Jun; 40(12):1828-36; ISSN: 1058-4838. 

Rec #: 1488 

 29. Tural, C.; Ruiz, L.; Holtzer, C.; Schapiro, J.; 

Viciana, P.; Gonzalez, J.; Domingo, P.; Boucher, 

C.; Rey-Joly, C., and Clotet, B. Clinical utility of 

HIV-1 genotyping and expert advice: the Havana 

trial. AIDS. 2002 Jan 25; 16(2):209-18. 

Rec #: 1550 

 30. Vray M; Meynard JL; Dalban C; Morand-Joubert L; 

Clavel F; Brun-Vezinet F; Peytavin G; Costagliola 

D; Girard PM, and Narval Trial Group (INSERM 

EMI 0214, Universite Pierre et Marie Curie, Paris, 

France. murielvray@hotmail.com). Predictors of the 

virological response to a change in the antiretroviral 

treatment regimen in HIV-1-infected patients 

enrolled in a randomized trial comparing 

genotyping, phenotyping and standard of care 

(Narval trial, ANRS 088). Antivir Ther. 2003 Oct; 

8(5):427-34. 

Rec #: 1369 

 31. Weidle, P.; Sozi, C.; Mwebaze, R., and et al. 

Resistance to antiretroviral therapy in the UNAIDS 

HIV drug access initiative-Uganda [abtract 527]. 

8th Conference on Retroviruses and Opportunistic 

Infections; Chicago. 2001. 

Rec #: 1598 

 32. Yahi, N.; Tamalet, C.; Tourres, C.; Tivoli, N., and 

Fantini, J. Mutation L210W of HIV-1 reverse 

transcriptase in patients receiving combination 

therapy. Incidence, association with other 

mutations, and effects on the structure of mutated 

reverse transcriptase. J Biomed Sci. 2000 Nov-2000 

Dec 31; 7(6):507-13. 

Rec #: 1256 
E-79 

Antiretroviral: Rejected : Second screening - Duplicate data 

 1. Adje-Toure, C.; Celestin, B.; Hanson, D.; Roels, T. 

H.; Hertogs, K.; Larder, B.; Diomande, F.; Peeters, 

M.; Eholie, S.; Lackritz, E.; Chorba, T., and 

Nkengasong, J. N. Prevalence of genotypic and 

phenotypic HIV-1 drug-resistant strains among 

patients who have rebound in viral load while 

receiving antiretroviral therapy in the UNAIDSDrug Access Initiative in Abidjan, Cote d'Ivoire. 

AIDS. 2003 Jul; 17 Suppl 3:S23-9. 

Rec #: 1088 

 2. Bauer, G. R.; Welles, S. L.; Colgrove, R. R., and 

Pitt, J. Zidovudine resistance phenotype and risk of 

perinatal HIV-1 transmission in zidovudine 

monotherapy-treated mothers with moderately 

advanced disease. J Acquir Immune Defic Syndr. 

2003 Nov 1; 34(3):312-9. 

Rec #: 1139 

 3. Eshleman, S. H.; Becker-Pergola, G.; Deseyve, M.; 

Guay, L. A.; Mracna, M.; Fleming, T.; 

Cunningham, S.; Musoke, P.; Mmiro, F., and 

Jackson, J. B. Impact of human immunodeficiency 

virus type 1 (hiv-1) subtype on women receiving 

single-dose nevirapine prophylaxis to prevent hiv-1 

vertical transmission (hiv network for prevention 

trials 012 study). J Infect Dis. 2001 Oct 1; 

184(7):914-7. 

Rec #: 1650 

 4. Eshleman, S. H.; Guay, L. A.; Mwatha, A.; 

Cunningham, S. P.; Brown, E. R.; Musoke, P.; 

Mmiro, F., and Jackson, J. B. Comparison of 

nevirapine (NVP) resistance in Ugandan women 7 

days vs. 6-8 weeks after single-dose nvp 

prophylaxis: HIVNET 012. AIDS Res Hum 

Retroviruses. 2004 Jun; 20(6):595-9. 

Rec #: 1036 

 5. Eshleman, S. H.; Hoover, D.; Chen, S.; Hudelson, 

S.; Guay, L.; Mwatha, A.; Brown, E.; Mmiro, F.; 

Musoke, P.; Jackson, J.; Kumwenda, N., and Taha, 

T. Comparison of Nevirapine Resistance in Women 

with Subtype C Compared with Subtypes A and D 

after Single-dose NVP. 12th Conference on 

Retroviruses and Opportunistic Infections; 2005. 

Rec #: 1898 

 6. Eshleman, S. H.; Hoover, D. R.; Hudelson, S. E.; 

Chen, S.; Guay, L. A.; Mwatha, A.; Fiscus, S. A.; 

Mmiro, F.; Musoke, P.; Jackson, J. B.; Kumwenda, 

N. I., and Taha, T. Resistance after single dose 

nevirapine prophylaxis varies by viral subtyle in 

infants from sub-Saharan Africa. Antivir Ther. 

2005; 10:S12. 

Rec #: 1954 

 7. Eshleman, S. H.; Hoover, D. R.; Hudelson, S. E.; 

Chen, S.; Mwatha, A.; Ficus, S. A.; Jackson, J. B.; 

Kumwenda, N. I., and Taha, T. Infant nevirapine 

resistance can be substantially reduced after single 

dose nevirapine by avoiding maternal nevirapine 

dosing and providing infants with zidovudine in 

addition to single dose nevirapine after birth. 

Antivir Ther. 2005; 10:S3. 

Rec #: 1953 

 8. Eshleman, S. H.; Mracna, M.; Guay, L. A.; 

Deseyve, M.; Cunningham, S.; Mirochnick, M.; 

Musoke, P.; Fleming, T.; Glenn Fowler, M.; 

Mofenson, L. M.; Mmiro, F., and Jackson, J. B. 

Selection and fading of resistance mutations in 

women and infants receiving nevirapine to prevent 

HIV-1 vertical transmission (HIVNET 012). AIDS. 

2001 Oct 19; 15(15):1951-7. 

Rec #: 1079 

 9. Flys, T. S.; Chen, S.; Jones, D.; Hoover, D.; Guay, 

L.; Jackson, J.; Fiscus, S.; Kumwenda, N.; Taha, T., 

and Eshleman, S. Analysis of K103N-containing 

HIV-1 Variants in Women with HIV-1 Subtypes A, 

C, and D after Single-dose Nevirapine Using a 

Sensitive and Quantitative Point Mutation Assay 

[Antiretroviral Resistance in Mother-to-child 

Transmission]. 13th Conference on Retroviruses 

and Opportunistic Infections; 2006. 

Rec #: 1779 

 10. Johnson, J.; Li, J. F.; Morris, L.; Martinson, N.; 

Gray, G.; McIntyre, J., and Heneine, W. Resistance 

Emerges in the Majority of Women Provided 

Intrapartum Single-dose Nevirapine. 12th 

Conference on Retroviruses and Opportunistic 

Infections; 2005. 

Rec #: 1830 

 11. Johnson, J. A.; Li, J-F; Morris, L.; Martinson, N.; 

Gray, G.; McIntyre, J., and Heneine, W. Resistance 

mutations arise in the majority of women provided 

single-dose NVP and appear to differ in emergence 

and persistence. Antivir Ther. 2005; 10:S13. 

Rec #: 1958 

 12. Nuesch, R.; Ananworanich, J.; Sirivichayakul, S.; 

Ubolyam, S.; Siangphoe, U.; Hill, A.; Cooper, D.; 

Lange, J.; Phanuphak, P., and Ruxrungtham, K. 

Development of HIV with drug resistance after 

CD4 cell count-guided structured treatment 

interruptions in patients treated with highly active 

antiretroviral therapy after dual-nucleoside analogue 

treatment. Clin Infect Dis. 2005 Mar 1; 40(5):728-

34. 

Rec #: 1467 
E-80 

 13. Palumbo, P.; Dobbs, T.; Holland, B., and et al. 

Antiretroviral resistance mutations among pregnant 

HIV-infected women and their newborns in the US: 

Vertical transmission and clades [abstract 

TuPpB1230]. XIII International AIDS Conference; 

Durban, South Africa. 2000. 

Rec #: 1603 

 14. Pieniazek, D.; Rayfield, M.; Hu, D. J.; Nkengasong, 

J.; Wiktor, S. Z.; Downing, R.; Biryahwaho, B.; 

Mastro, T.; Tanuri, A.; Soriano, V.; Lal, R., and 

Dondero, T. Protease sequences from HIV-1 group 

M subtypes A-H reveal distinct amino acid 

mutation patterns associated with protease 

resistance in protease inhibitor-naive individuals 

worldwide. HIV Variant Working Group. AIDS. 

2000 Jul 28; 14(11):1489-95. 

Rec #: 1207 
E-81 

Antiretroviral: Rejected : Second screening - Insufficient 

statistics 

 1. Easterbrook, P. J.; Hertogs, K.; Waters, A.; Wills, B.; 

Gazzard, B. G., and Larder, B. Low prevalence of 

antiretroviral drug resistance among HIV-1 

seroconverters in London, 1984-1991. J Infect. 2002 

Feb; 44(2):88-91. 

Rec #: 1180 

 2. Harrigan, P. R.; Montaner, J. S.; Wegner, S. A.; 

Verbiest, W.; Miller, V.; Wood, R., and Larder, B. A. 

World-wide variation in HIV-1 phenotypic 

susceptibility in untreated individuals: biologically 

relevant values for resistance testing. AIDS. 2001 Sep 

7; 15(13):1671-7. 

Rec #: 2067 

 3. Johnson, M.; DeJesus, E.; Rodriguez, C.; NietoCisneros, L. ; Rightmire, A.; McLaren, C., and 

Odeshoo, L. The Influence of Baseline Protease 

Inhibitor Mutations on the Efficacy of RitonavirBoosted Atazanavir, Atazanavir plus Saquinavir, and 

Lopinavir/Ritonavir in Patients Who Have 

Experienced Virologic Failure on Multiple HAART 

Regimens. 12th Conference on Retroviruses and 

Opportunistic Infections; 2005. 

Rec #: 1851