bluuebunny/crossref_metadata_2025_split huggingface dataset:
Performance of two commercially available sequence‐based HIV‐1 genotyping systems for the detection of drug resistance against HIV type 1 group M subtypes
Authors: Beddows Simon , Galpin Sarah , Kazmi Shamim H. , Ashraf Ambreen , Johargy Ayman , Frater Alexander J. , White Natalie , Braganza Ruth , Clarke John , McClure Myra , Weber Jonathan N. 
Published: May 2003

AbstractThe use of genotyping assays for the detection and evaluation of drug resistance mutations within the polymerase gene of human immunodeficiency virus type 1 (HIV‐1) is becoming increasingly relevant in the clinical management of HIV‐1 infection. However, genotypic resistance assays available currently have been optimised for genetic subtype B strains of the virus and many clinical centres are presented with strains from subtypes A, C, and D. In the present report, we compare the performance of two sequence‐based commercially available kits, the ViroSeq Genotyping System (Applied Biosystems, Foster City, CA) and the TruGene HIV‐1 Genotyping Kit (Visible Genetics, Toronto, Ontario) against a panel of 35 virus isolates from HIV‐1 Group M (subtypes A–J). Full‐length consensus sequences were generated by the ViroSeq genotyping system for 26 of 31 (83.8%) of the isolates tested, in contrast to the TruGene genotyping system, which generated 16 of 30 (53%) usable sequences overall. Overall, subtype B isolates were sequenced with a greater degree of success than non‐subtype B isolates. Discrepancies were found between the consensus sequences reported by each system for each sample (mean difference 1.0%; range 0.0–3.2%), but these appeared to be random and did not affect interpretation of the major resistance codons. In addition, both systems were able to amplify template RNA from low copy viral load plasma samples (102–103 RNA copies/ml) taken from a random selection of patient samples encompassing subtypes A–C. While the availability of these genotyping systems should facilitate studies of HIV‐1 drug resistance in countries in which these subtypes are prevalent, the performance against subtypes other than B needs to be improved. J. Med. Virol. 70:337–342, 2003. © 2003 Wiley‐Liss, Inc.
Genetic analysis of HAV strains recovered from patients with acute hepatitis from Southern Italy
Authors: Chironna Maria , Grottola Antonella , Lanave Cecilia , Villa Erica , Barbuti Salvatore , Quarto Michele 
Published: May 2003

AbstractSouthern Italy is an endemic area for HAV infection contributing to the majority of Italian hepatitis A cases. Using molecular analysis, HAV strains have been classified in distinct genotypes and subgenotypes. To characterize HAV wild‐type strains circulating in Southern Italy, sequence analysis of VP3‐VP1 and VP1/2A junction regions of HAV isolates recovered from 25 patients with acute hepatitis during 2000 and 2001 was carried out. HAV isolates showed a degree of identity, after pairwise comparison with one another, ranging from 91.9–100% in the VP3‐VP1 junction region and 89.9–100% in the VP1/2A junction region. All strains belonged to genotype I, with 84% (21/25) of samples clustering in subgenotype IA and 16% (4/25) in subgenotype IB. Cocirculation of subgenotypes IA and IB was observed among isolates from 2000, whereas all strains from 2001 were subgenotype IA. In addition, the subgenotype IA strains formed different clusters, one of which was related closely to some Cuban strains, showing a percent similarity of 98.8% in the 168‐base pair segment encompassing the VP1/2A junction and the same amino acid substitution. The latter finding suggests that this subgenotype variant circulates also in the Mediterranean area. The results of the phylogenetic analysis confirm the genetic heterogeneity among HAV strains in Western Europe. J. Med. Virol. 70:343–349, 2003. © 2003 Wiley‐Liss, Inc.
HBe antigen loss during lamivudine therapy is not caused by mutations in precore and core promoter genes in patients with chronic hepatitis B
Authors: Suzuki Fumitaka , Tsubota Akihito , Arase Yasuji , Suzuki Yoshiyuki , Akuta Norio , Hosaka Tetsuya , Someya Takashi , Kobayashi Masahiro , Saitoh Satoshi , Ikeda Kenji , Kobayashi Mariko , Matsuda Marie , Satoh Junko , Takagi Kimiko , Kumada Hiromitsu 
Published: May 2003

AbstractHBe antigen (HBeAg) loss or seroconversion can occur during lamivudine therapy. The purpose of this study was to analyze nucleotide sequences in precore and core promoter regions, and examine the influence of mutations in these regions on the disappearance of HBeAg during lamivudine therapy. Serial serum samples were obtained from 51 patients (HBeAg loss in 26 patients) at commencement of therapy (baseline) and after 1 year of lamivudine therapy. Serum samples were amplified with PCR and nucleotide sequences of HBV were analyzed. At baseline, a precore stop codon mutation (A1896) was identified in 8 of 26 HBeAg loss patients and in 8 of 25 HBeAg non‐loss patients. At 1 year, precore mutation was observed in 4 of 14 patients analyzed who showed HBeAg loss. At 1 year, however, a precore mutation was observed also in 3 of 9 analyzed patients who showed no HBeAg loss. Core promoter mutations were noted in 21 of 26 HBeAg loss patients and in 20 of 25 HBeAg non‐loss patients. At 1 year, core promoter mutations were noted in 11 of 14 HBeAg loss patients and in 8 of 9 HBeAg non‐loss patients. Our data suggested that during lamivudine therapy, core promoter and precore mutations do not influence HBeAg loss or seroconversion but may reduce the viral level upon HBeAg loss or seroconversion. J. Med. Virol. 70:355–360, 2003. © 2003 Wiley‐Liss, Inc.
Characterisation of the differences between hepatitis C virus genotype 3 and 1 glycoproteins
Authors: Shaw Megan L. , McLauchlan John , Mills Peter R. , Patel Arvind H. , McCruden Elizabeth A.B. 
Published: May 2003

AbstractSequence variation in the envelope E1 and E2 glycoproteins of hepatitis C virus (HCV) could account for differences in disease pathogenesis in patients infected with different genotypes. A cDNA encoding the structural region of the hepatitis C polyprotein was constructed to match the majority sequence of viral RNA extracted from a patient infected with genotype 3a (designated strain HCV3a‐Gla). The principal differences predicted between E2 of HCV3a‐Gla and the corresponding H77c genotype 1a protein were that the former contained six more amino acids (361 vs. 355), but it had one fewer glycosylation site. Expression studies showed that, in common with the H77c glycoproteins, E1 and E2 from HCV3a‐Gla localised to the endoplasmic reticulum (ER) membrane in both Huh‐7 and BHK tissue culture cells and interacted to form native complexes. Analysis of the cross‐reactivity of antibodies raised against glycoproteins of genotype 1a strains showed that three of five monoclonal antibodies that recognise linear epitopes were able to detect E2 from strain HCV3a‐Gla. However, neither conformational E2 antibodies nor antibodies raised against E1 were able to detect the HCV3a‐Gla glycoproteins. In receptor binding assays, E2 of HCV3a‐Gla consistently failed to bind CD81, a putative cell receptor for HCV. Absence of binding to CD81 and lack of recognition by most antibodies raised to genotype 1a glycoproteins indicate important differences between these glycoproteins representative of genotypes 3a and 1a. These may be pertinent to the differences in response to interferon therapy and the prevalence of steatosis reported in patients infected with these genotypes. J. Med. Virol. 70:361–372, 2003. © 2003 Wiley‐Liss, Inc.
Clinical features and progression of perinatally acquired hepatitis C virus infection
Authors: Resti Massimo , Jara Paloma , Hierro Loreto , Azzari Chiara , Giacchino Raffaella , Zuin Giovanna , Zancan Lucia , Pedditzi Sabrina , Bortolotti Flavia 
Published: May 2003

AbstractThe purpose of this prospective‐retrospective study was to provide information about the clinical features and progression of hepatitis C virus (HCV) infection transmitted perinatally. Seventy children born to HCV infected woman were enrolled consecutively in five European centers between 1990 and 1999, provided they had HCV RNA in the serum during the first year of life and/or were still anti‐HCV positive at 18 months. Sixty‐two infants were followed up to 24 months of age or more (range, 24 months–11 years; average, 4.8 ± 2.3 years). A wide range of ALT elevation was observed in 93% of the infants in the first year of life. During the follow‐up, a sustained ALT normalization with loss of HCV RNA was seen in 12/62 (19%) of the children within 30 months of life; 66% of the infants had developed an ALT peak greater than 5× normal at onset (vs. 28% of children with persistent viremia; P < 0.05), and 50% had HCV genotype 3 (vs. 17% of viremic children). Conversely the cumulative probability of chronic progression was 81%. Chronic infection was asymptomatic and liver disease was mild in all 11 children who underwent a biopsy. In conclusion the early stage of acquired perinatally HCV infection is characterized by a wide range of ALT abnormalities, suggesting the interaction of multiple host and virus factors. The chronic progression rate of infection is high, but the associated liver disease is usually mild. High ALT levels at onset seem to offer greater opportunity of biochemical remission and loss of viremia during follow‐up. J. Med. Virol. 70:373–377, 2003. © 2003 Wiley‐Liss, Inc.
Natural histories of hepatitis C virus infection in men and women simulated by the Markov model
Authors: Tanaka Junko , Kumada Hiromitsu , Ikeda Kenji , Chayama Kazuaki , Mizui Masaaki , Hino Kunihiko , Katayama Keiko , Kumagai Junko , Komiya Yutaka , Miyakawa Yuzo , Yoshizawa Hiroshi 
Published: May 2003

AbstractThe Markov model was introduced to simulate natural histories of hepatitis C virus (HCV) infection in men and women. The data set was constructed on 942 HCV carriers who were examined at least once a year without receiving antiviral therapies. Based on 2,251 patient‐year data, the probabilities of transition between any two of the four clinical states, i.e., asymptomatic carrier state, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma in 1 year were calculated. Hepatocellular carcinoma was defined as the absorbing state from where no transitions occur. Probability matrices thus obtained on six each subsets of HCV infection (asymptomatic carrier state, chronic hepatitis and liver cirrhosis in men and women) in their forties, fifties, and sixties, were used to simulate long‐term outcomes of HCV infection. Male asymptomatic carriers aged 40 years were expected to retain the asymptomatic carrier state in 2.6%, evolve into chronic hepatitis in 48.4%, liver cirrhosis in 14.6% and hepatocellular carcinoma in 34.4% after 30 years when they reached 70 years of age, in contrast to 1.9%, 45.3%, 32.8% and 20.0%, respectively, of female asymptomatic carriers. Likewise, male patients with chronic hepatitis aged 40 years were expected to remain with chronic hepatitis in 43.8%, evolve into liver cirrhosis in 15.0% and hepatocellular carcinoma in 41.1%, contrasting with 38.9%, 32.7% and 22.0%, respectively, of female patients during 30 years. The Markov model could simulate the outcomes of 153 HCV carriers identified among blood donors after 5 years. The Markov simulation would help in assessing the long‐term outcome of HCV infection and making decisions in the management of HCV carriers toward prevention of hepatocellular carcinoma. J. Med. Virol. 70:378–386, 2003. © 2003 Wiley‐Liss, Inc.
Hepatitis C virus infection among noninjecting drug users in New York City
Authors: Koblin Beryl A. , Factor Stephanie H. , Wu Yingfeng , Vlahov David 
Published: May 2003

AbstractThe prevalence of hepatitis C virus (HCV) infection among noninjecting drug users has been reported to be higher than in the general population, but the reasons for this observation remain unclear. Noninjecting drug users aged 15–40 years and who used drugs for no longer than 10 years were enrolled in the study. The participants were interviewed about risk behaviors and had specimens drawn for serological testing. Of 276 enrolled, 4.7% were infected with HCV. Drug users who had ever sniffed or snorted heroin in combination with cocaine were significantly more likely to be infected with HCV compared with those who never sniffed or snorted heroin with cocaine. No other drug use or sexual risk behaviors were found to be associated with HCV infection. These findings suggest that sniffing or snorting heroin with cocaine may explain the increase frequently found in HCV infection among noninjectors, but further studies are necessary. J. Med. Virol. 70:387–390, 2003. © 2003 Wiley‐Liss, Inc.
Sialic acid receptor specificity on erythrocytes affects detection of antibody to avian influenza haemagglutinin
Authors: Stephenson I. , Wood J.M. , Nicholson K.G. , Zambon M.C. 
Published: May 2003

AbstractHaemagglutination‐inhibition tests (HI) are used to detect increases in influenza antibody in serum. However, they are relatively insensitive for the detection of human antibody responses to avian haemagglutinin, even in the presence of high titres of neutralising antibody after confirmed infection or vaccination. Human influenza viruses bind preferentially sialic acid containing N‐acetylneuraminic acid α2,6‐galactose (SAα2,6Gal) linkages while avian and equine viruses bind preferentially those containing N‐acetylneuraminic acid α2,3‐galactose (SAα2,3Gal) linkages. Increasing the proportion of SAα2,3Gal linkages on the erythrocytes used, by enzymatic modification or change of species, improves the ability of erythrocytes to bind to avian influenza strains and thereby improves the sensitivity of detection of antibody to avian and equine HA in a range of mammalian and human sera using HI tests. J. Med. Virol. 70:391–398, 2003. © 2003 Wiley‐Liss, Inc.
Reconstitution of lymphocyte populations and cytomegalovirus viremia or disease after allogeneic peripheral blood stem cell transplantation
Authors: Gutiérrez Antonio , Muñoz Isabel , Solano Carlos , Benet Isabel , Gimeno Concepción , Marugán Isabel , Gea María Dolores , García‐Conde Javier , Navarro David 
Published: May 2003

AbstractEarly reconstitution of lymphoid populations was monitored by immunophenotyping in 57 allogeneic peripheral blood stem cell (allo‐PBSC) transplant patients either with or without cytomegalovirus (CMV) viremia or disease. Cell counts for total lymphocytes and CD4+ T cells above the percentile 60th at day 14 postransplant were associated significantly with CMV viremia‐free survival within 120 days after transplant. Recovery of total lymphocyte, CD3+, and CD8+ T‐cell counts proceeded at a more rapid rate in CMV viremic patients than in nonviremic patients, irrespective of whether preemptive treatment with ganciclovir had been prescribed. Significant expansion of CD8+ and CD8+ CD57+ T‐cell subsets was associated with recovery from viremia and no progression to CMV disease. Immunophenotyping may provide useful information for the clinical management of CMV infection in allo‐PBSC transplant recipients. J. Med. Virol. 70:399–403, 2003. © 2003 Wiley‐Liss, Inc.
Molecular epidemiological study of dengue virus type 1 in Taiwan
Authors: Hwang Kao‐Pin , Chu Pei‐Yu , Tung Yi‐Ching , Wang Heng‐Lin , Yueh Yi‐Yun , Wu Ying‐Chang , Chin Chuan , Lin Kuei‐Hsiang 
Published: May 2003

AbstractTaiwan has experienced several major outbreaks of dengue (DEN) virus since 1981. The predominant virus type involved has been dengue virus type one (DEN‐1), which first appeared in 1987. To understand the molecular epidemiology of this virus, 15 strains of DEN‐1 isolated during 1987–1991 and 1994–1995, including 11 epidemic strains, two sporadic strains, and two imported strains have been studied. Fragments of 490 nucleotides (nt) from the E/NS1 junction were amplified by reverse transcription‐polymerase chain reaction and the nt sequences were determined. Of the 490 nt of the E/NS1 junction, 240 nt (nt 2282–2521) were aligned and compared. Nucleotide substitutions were found at 54 positions among 15 isolates. Most nt changes were synonymous substitutions, and only three amino acid changes were found. A total of 61 strains isolated worldwide were analyzed by the Neighbor‐joining method, and separated phylogenetically into three distinct genotypes, I–III. Genotype I comprised isolates from Japan and Hawaii collected in the 1940s. Genotype II included most strains isolated from Asia in 1977–1995. Genotype III consisted of isolates from three continents in 1964–1995: Asia, the Americas, and Africa. Genotype III was divided further into two subgenotypes, IIIA and IIIB. Most recent isolates from Taiwan, except for the sporadic strain isolated in 1995, were similar genetically and have been classified as Genotype II. J. Med. Virol. 70:404–409, 2003. © 2003 Wiley‐Liss, Inc.
Latency pattern of Epstein‐Barr virus and methylation status in Epstein‐Barr virus‐associated hemophagocytic syndrome
Authors: Yoshioka Mikio , Kikuta Hideaki , Ishiguro Nobuhisa , Endo Rika , Kobayashi Kunihiko 
Published: May 2003

AbstractExpression of different panels of latent gene transcripts is controlled by usage of three distinct Epstein‐Barr virus (EBV) nuclear antigen (EBNA) promoters (Wp, Cp, and Qp). EBV‐associated hemophagocytic syndrome, which is often a fatal disease and generally occurs after primary EBV infection, is characterized by monoclonal or oligoclonal proliferation of EBV‐infected T cells. The latency pattern and EBNA promoter (Wp, Cp, and Qp) usage in EBV‐infected cells from three patients with EBV‐associated hemophagocytic syndrome were examined by reverse transcription‐polymerase chain reaction (PCR). Three samples from the patients expressed EBER, EBNA1, EBNA2, latent membrane protein (LMP)1, and LMP2A transcripts. The transcripts of EBNA1 were initiated from not only Wp/Cp but also Qp. Lytic cycle Fp‐initiated EBNA1 and EBV lytic gene BZLF1 transcripts were not detected. The methylation statuses of three EBNA promoters in three patients with EBV‐associated hemophagocytic syndrome and in two patients with infectious mononucleosis were also analyzed using bisulfite PCR analysis. Wp was hypermethylated, and Qp was unmethylated in both diseases. Cp was highly methylated in EBV‐associated hemophagocytic syndrome, however, whereas Cp was almost unmethylated in infectious mononucleosis. These results suggest that there may be distinct EBV‐infected cell populations in EBV‐associated hemophagocytic syndrome, which exhibit different patterns of EBV latent gene expression. The methylation status in Cp and phenotype of EBV‐infected cells may be critical differences in EBV‐associated hemophagocytic syndrome and infectious mononucleosis. J. Med. Virol. 70:410–419, 2003. © 2003 Wiley‐Liss, Inc.
Molecular typing and epidemiology of enteroviruses identified from an outbreak of aseptic meningitis in Belgium during the summer of 2000
Authors: Thoelen Inge , Lemey Philippe , Van der Donck Ingrid , Beuselinck Kurt , Lindberg A. Michael , Van Ranst Marc 
Published: May 2003

AbstractNon‐polio enteroviruses are the most common cause of aseptic meningitis worldwide. From May to September 2000, a major outbreak of aseptic meningitis occurred in Belgium. Cerebrospinal fluid samples (CSF) of 122 patients were found to contain enterovirus RNA using diagnostic RT‐PCR that targeted a 231‐bp gene fragment in the 5′ noncoding region. In addition, a molecular typing method was developed based on RT‐nested PCR and sequencing directly from CSFa 358‐bp fragment in the aminoterminal part of the VP1 capsid protein. To identify the enterovirus type, nucleotide sequences of the VP1 amplicons were compared to all the enterovirus VP1 sequences available in GenBank. Echovirus 30 (31.2%), echovirus 13 (23.8%), and echovirus 6 (20.5%) were identified most frequently during the epidemic. Coxsackievirus B5 was present in 15.6% of the samples, and could be subdivided in two distinct epidemic clusters, coxsackievirus B5a (10.7%) and B5b (4.9%). Other enteroviruses encountered were echovirus 16 (5.7%), echovirus 18 (1.6%), coxsackievirus B4 (0.8%) and echovirus 7 (0.8%). The high prevalence of echovirus 13, considered previously a rare serotype, indicates it is an emerging epidemic type. To verify the typing results and to explore further the intratypical genetic variation, phylogenetic analysis was carried out. Geographical clustering of most of the strains within each type and subtype could be observed. The RT‐nested PCR strategy, carried out directly on clinical samples, is a simple and rapid method for adequate molecular typing of the Group B enteroviruses causing aseptic meningitis. J. Med. Virol. 70:420–429, 2003. © 2003 Wiley‐Liss, Inc.
Enterovirus infection and activation of human umbilical vein endothelial cells
Authors: Saijets Salla , Ylipaasto Petri , Vaarala Outi , Hovi Tapani , Roivainen Merja 
Published: May 2003

AbstractGastrointestinal tract associated lymphoid tissue is considered to be the main replication site for enteroviruses. In order to invade tissues to reach pancreatic islets, cardiac muscles, and other secondary replication sites, the virus has to survive circulation in the blood and find a way to get through endothelial cells. In the present study, the susceptibility of human endothelial cells to infections caused by human parechovirus 1 and several prototype strains of enteroviruses, representing different species (human poliovirus, human enterovirus B and C), and acting through different receptor families was examined. Primary endothelial cells isolated from human umbilical vein by collagenase perfusion and also an established human endothelial cell line, HUVEC, were used. Primary endothelial cells were highly susceptible to several serotypes of enteroviruses (coxsackievirus A13, echoviruses 6, 7, 11, 30, and poliovirus 1). However, coxsackievirus A 9 and echovirus 1 infected only a few individual cells while human parechovirus 1 and coxsackie B viruses did not show evidence of replication in primary endothelial cells. In general, primary endothelial cells were more sensitive to infection‐induced cytolytic effect than HUVEC. Activation of endothelial cells by interleukin‐1β did not change the pattern of enterovirus infection. Immunofluorescence stainings of infected primary endothelial cells showed that expression of activation markers, E‐selectin, and intercellular adhesion molecule‐1, was clearly increased by several virus infections and the former molecule also by exposing cells to UV‐light inactivated coxsackieviruses. In contrast, human leukocyte antigen‐DR expression was not increased by virus infection. J. Med. Virol. 70:430–439, 2003. © 2003 Wiley‐Liss, Inc.
Human herpesvirus 7‐associated meningitis and optic neuritis in a patient after allogeneic stem cell transplantation
Authors: Yoshikawa Tetsushi , Yoshida Jun , Hamaguchi Motohiro , Kubota Toshinobu , Akimoto Shiho , Ihira Masaru , Nishiyama Yukihiro , Asano Yoshizo 
Published: May 2003

AbstractA 9‐year‐old boy who received allogeneic stem cell transplantation began to vomit from day 10 after transplantation. In addition to vomiting, the patient had a fever (from day 26) and severe headache (from day 34). His cerebrospinal fluid (CSF) (day 41) demonstrated pleocytosis with an absence of leukemic cells. Although the patient's symptoms were resolved with further supportive care, abrupt onset of bilateral decreased vision occurred at day 54. He was diagnosed with bilateral optic neuritis, due to the presence of disc edema and redness. Concomitant with the occurrence of aseptic meningitis, the human herpesvirus 7 (HHV‐7) antibody titer increased significantly in this patient. Although neither HHV‐6 nor cytomegalovirus (CMV) DNA was detected in CSF collected at day 41, HHV‐7 DNA was detected in the sample. Viral DNA was not detected in CSF collected at day 93. J. Med. Virol. 70:440–443, 2003. © 2003 Wiley‐Liss, Inc.