bluuebunny/crossref_metadata_2025_split huggingface dataset:
Treatment Failure Related to Intrathecal Immunoglobulin M (IgM) Synthesis, Cerebrospinal Fluid IgM, and Interleukin-10 in Patients with Hemolymphatic-Stage Sleeping Sickness
Authors: Lejon Veerle , Robays Jo , N'Siesi François Xavier , Mumba Dieudonné , Hoogstoel Annemie , Bisser Sylvie , Reiber Hansotto , Boelaert Marleen , Büscher Philippe 
Published: April 2007

ABSTRACT

Human African trypanosomiasis treatment is stage dependent, but the tests used for staging are controversial. Central nervous system involvement and its relationship with suramin treatment failure were assessed in 60 patients with parasitologically confirmed hemolymphatic-stage
Trypanosoma brucei gambiense
infection (white blood cell count of ≤5/μl and no trypanosomes in the cerebrospinal fluid [CSF]). The prognostic value of CSF interleukin-10, immunoglobulin M (IgM; as determined by nephelometry and the point-of-care LATEX/IgM test), total protein, and trypanosome-specific antibody was assessed. The IgM and interleukin-10 levels in serum were measured; and the presence of neurological signs, intrathecal IgM synthesis, and blood-CSF barrier dysfunction was determined. After suramin treatment, 14 of 60 patients had relapses (23%). Relapses were significantly correlated with intrathecal IgM synthesis (odds ratio [OR], 46; 95% confidence interval [CI], 8 to 260), a CSF IgM concentration of ≥1.9 mg/liter (OR, 11.7; 95% CI, 2.7 to 50), a CSF end titer by the LATEX/IgM assay of ≥2 (OR, 10.4; 95% CI, 2.5 to 44), and a CSF interleukin-10 concentration of >10 pg/ml (OR, 5; 95% CI, 1.3 to 20). The sensitivities of these markers for treatment failure ranged from 43 to 79%, and the specificities ranged from 74 to 93%. The results show that
T. brucei gambiense
-infected patients who have signs of neuroinflammation in CSF and who are treated with drugs recommended for use at the hemolymphatic stage are at risk of treatment failure. This highlights the need for the development and the evaluation of accurate point-of-care tests for the staging of human African trypanosomiasis.
Identification and Distribution of
Mycobacterium leprae
Genotypes in a Region of High Leprosy Prevalence in China: a 3-Year Molecular Epidemiological Study
Authors: Weng Xiaoman , Wang Zheng , Liu Jian , Kimura Miyako , Black William C. , Brennan Patrick J. , Li Huanying , Vissa Varalakshmi D. 
Published: April 2007

ABSTRACT

Multiple-locus variable-number tandem-repeat (VNTR) analysis (MLVA) has been proposed as a means of strain typing for tracking the transmission of leprosy. However, empirical data for a defined population are lacking. To this end, a study was initiated to assess the diversity and distribution of prevalent
Mycobacterium leprae
strains in Qiubei County, Yunnan Province, People's Republic of China, where the annual detection rate of leprosy is 10-fold higher than the national average rate. Sixty-eight newly diagnosed leprosy patients were included in the study. MLVA at eight
M. leprae
loci was applied using DNA extracts from skin biopsies. The number of alleles per locus ranged from 4 to 24, providing adequate strain discrimination. MLVA strain typing identified several clusters of patients whose
M. leprae
specimens shared similar VNTR profiles. Two of these clusters were comprised of patients who resided predominantly in the north and northwest parts of Qiubei County. Furthermore, it was found that multicase families are common in this county: 23 of the 68 patients were from 11 families. Intrafamilial VNTR profiles closely matched within six families, although they were different between the families. Moreover, VNTR patterns related to those found in some multicase families were also detected in patients in the same or adjacent townships, indicating the utility of VNTR strain typing to identify and detect short-range transmission events. Social contact through village markets is proposed as a means of transmission.
Bronchoalveolar Lavage Galactomannan in Diagnosis of Invasive Pulmonary Aspergillosis among Solid-Organ Transplant Recipients
Authors: Clancy Cornelius J. , Jaber Reia A. , Leather Helen L. , Wingard John R. , Staley Benjamin , Wheat L. Joseph , Cline Christina L. , Rand Kenneth H. , Schain Denise , Baz Maher , Nguyen M. Hong 
Published: April 2007

ABSTRACT
We review the experience at our institution with galactomannan (GM) testing of bronchoalveolar lavage (BAL) fluid in the diagnosis of invasive pulmonary aspergillosis (IPA) among solid-organ transplant recipients. Among 81 patients for whom BAL GM testing was ordered (heart, 24; kidney, 22; liver, 19; lung, 16), there were five cases of proven or probable IPA. All five patients had BAL GM of ≥2.1 and survived following antifungal therapy. The sensitivity, specificity, and positive and negative predictive values for BAL GM testing at a cutoff of ≥1.0 were 100%, 90.8%, 41.7%, and 100%, respectively. The sensitivity of BAL GM testing was better than that of conventional tests such as serum GM or BAL cytology and culture. Moreover, a positive BAL GM test diagnosed IPA several days to 4 weeks before other methods for three patients. Twelve patients had BAL GM of ≥0.5 but no evidence of IPA. Among these, lung transplant recipients accounted for 41.7% (5/12) of the false-positive results, reflecting frequent colonization of airways in this population. Excluding lung transplants, the specificity and positive predictive value for other solid-organ transplants increased to 92.9% and 62.5%, respectively (cutoff, ≥1.0). In conclusion, BAL GM testing facilitated more-rapid diagnoses of IPA and the institution of antifungal therapy among non-lung solid-organ transplant recipients and helped to rule out IPA.
Analysis of the First Australian Strains of
Bartonella quintana
Reveals Unique Genotypes
Authors: Woolley Mark W. , Gordon David L. , Wetherall Bruce L. 
Published: April 2007

ABSTRACT

Bartonella quintana
is increasingly recognized as a cause of clinical disease in various geographical locations. We characterized three Australian strains associated with endocarditis, using established molecular-typing techniques, the 16S/23S rRNA intergenic spacer (ITS) region, and multispacer typing (MST). All strains examined demonstrated novel ITS and/or MST genotypes. Further characterization of Australian strains is required to determine whether there is an association between genotype and geographical location.
Peptoniphilus gorbachii
sp. nov.,
Peptoniphilus olsenii
sp. nov., and
Anaerococcus murdochii
sp. nov. Isolated from Clinical Specimens of Human Origin
Authors: Song Yuli , Liu Chengxu , Finegold Sydney M. 
Published: April 2007

ABSTRACT

Three groups of previously unknown gram-positive, anaerobic, coccus-shaped bacteria were characterized using phenotypic and molecular taxonomic methods. Phenotypic and genotypic data demonstrate that these organisms are distinct, and each group represents a previously unknown subline within
Clostridium
cluster XIII. Two groups are most closely related to
Peptoniphilus harei
in the genus
Peptoniphilus
, and the other group is most closely related to
Anaerococcus lactolyticus
in the genus
Anaerococcus
. Based on the findings, three novel species,
Peptoniphilus gorbachii
sp. nov.,
Peptoniphilus olsenii
sp. nov., and
Anaerococcus murdochii
sp. nov., are proposed. The type strains of
Peptoniphilus gorbachii
sp. nov.,
Peptoniphilus olsenii
sp. nov., and
Anaerococcus murdochii
sp. nov. are WAL 10418
T
(= CCUG 53341
T
= ATCC BAA-1383
T
), WAL 12922
T
(= CCUG 53342
T
= ATCC BAA-1384
T
), and WAL 17230
T
(= CCUG 53340
T
= ATCC BAA-1385
T
), respectively.
Outbreak of Fungemia among Neonates Caused by
Candida haemulonii
Resistant to Amphotericin B, Itraconazole, and Fluconazole
Authors: Khan Zia U. , Al-Sweih Noura A. , Ahmad Suhail , Al-Kazemi Nawal , Khan Seema , Joseph Leena , Chandy Rachel 
Published: April 2007

ABSTRACT

The first outbreak of
Candida haemulonii
fungemia is described. The seven isolates from the blood of four neonates were identified by DNA sequencing of the ribosomal DNA. They were all resistant to amphotericin B, fluconazole, and itraconazole. This report highlights the emergence of
C. haemulonii
as an opportunistic pathogen in immunocompromised patients.
Performance of a Rapid Assay (Binax NOW) for Detection of Respiratory Syncytial Virus at a Children's Hospital over a 3-Year Period
Authors: Cruz Andrea T. , Cazacu Andreea C. , Greer Jewel M. , Demmler Gail J. 
Published: April 2007

ABSTRACT

A rapid assay, Binax NOW RSV, was compared to viral culture for 14,756 pediatric respiratory specimens obtained from 2003 to 2006. There were 794 viral culture-confirmed respiratory syncytial virus infections. Sensitivity was 81%, and specificity was 93.2%. Sensitivity was greatest for neonates (91.1% versus 80.7% [
P
< 0.01]).
Clinical Evaluation of the Sensititre YeastOne Plate for Testing Susceptibility of Filamentous Fungi to Posaconazole
Authors: Patel Reena , Mendrick Cara , Knapp Cindy C. , Grist Roger , McNicholas Paul M. 
Published: April 2007

ABSTRACT

Sensititre YeastOne colorimetric antifungal panels were compared with the CLSI (formerly NCCLS) M38-A reference method for testing the susceptibility of filamentous fungi to posaconazole; agreement (±2 log
2
dilutions) between the two methods was 97%. These data confirm the utility of YeastOne panels for measuring the susceptibility of filamentous fungi to posaconazole.
PCR-Restriction Fragment Length Polymorphism for Rapid, Low-Cost Identification of Isoniazid-Resistant
Mycobacterium tuberculosis
Authors: Caws Maxine , Tho Dau Quang , Duy Phan Minh , Lan Nguyen Thi Ngoc , Hoa Dai Viet , Torok Mili Estee , Chau Tran Thi Hong , Van Vinh Chau Nguyen , Chinh Nguyen Tran , Farrar Jeremy 
Published: April 2007

ABSTRACT

PCR-restriction fragment length poymorphism (PCR-RFLP) is a simple, robust technique for the rapid identification of isoniazid-resistant
Mycobacterium tuberculosis
. One hundred consecutive isolates from a Vietnamese tuberculosis hospital were tested by MspA1I PCR-RFLP for the detection of isoniazid-resistant
katG
_315 mutants. The test had a sensitivity of 80% and a specificity of 100% against conventional phenotypic drug susceptibility testing. The positive and negative predictive values were 1 and 0.86, respectively. None of the discrepant isolates had mutant
katG
_315 codons by sequencing. The test is cheap (less than $1.50 per test), specific, and suitable for the rapid identification of isoniazid resistance in regions with a high prevalence of
katG
_315 mutants among isoniazid-resistant
M. tuberculosis
isolates.
Analysis of Murine Hepatitis Virus Strain A59 Temperature-Sensitive Mutant TS-LA6 Suggests that nsp10 Plays a Critical Role in Polyprotein Processing
Authors: Donaldson Eric F. , Graham Rachel L. , Sims Amy C. , Denison Mark R. , Baric Ralph S. 
Published: April 2007

ABSTRACT
Coronaviruses are the largest RNA viruses, and their genomes encode replication machinery capable of efficient replication of both positive- and negative-strand viral RNAs as well as enzymes capable of processing large viral polyproteins into putative replication intermediates and mature proteins. A model described recently by Sawicki et al. (S. G. Sawicki, D. L. Sawicki, D. Younker, Y. Meyer, V. Thiel, H. Stokes, and S. G. Siddell, PLoS Pathog. 1:e39, 2005), based upon complementation studies of known temperature-sensitive (TS) mutants of murine hepatitis virus (MHV) strain A59, proposes that an intermediate comprised of nsp4 to nsp10/11 (∼150 kDa) is involved in negative-strand synthesis. Furthermore, the mature forms of nsp4 to nsp10 are thought to serve as cofactors with other replicase proteins to assemble a larger replication complex specifically formed to transcribe positive-strand RNAs. In this study, we introduced a single-amino-acid change (nsp10:Q65E) associated with the TS-LA6 phenotype into nsp10 of the infectious clone of MHV. Growth kinetic studies demonstrated that this mutation was sufficient to generate the TS phenotype at permissive and nonpermissive temperatures. Our results demonstrate that the TS mutant variant of nsp10 inhibits the main protease, 3CLpro, blocking its function completely at the nonpermissive temperature. These results implicate nsp10 as being a critical factor in the activation of 3CLpro function. We discuss how these findings challenge the current hypothesis that nsp4 to nsp10/11 functions as a single cistron in negative-strand RNA synthesis and analyze recent complementation data in light of these new findings.
Epstein-Barr Virus Thymidine Kinase Is a Centrosomal Resident Precisely Localized to the Periphery of Centrioles
Authors: Gill Michael B. , Kutok Jeffery L. , Fingeroth Joyce D. 
Published: April 2007

ABSTRACT
The thymidine kinase (TK) encoded by Epstein-Barr virus (EBV) differs not only from that of the alphaherpesviruses but also from that of the gamma-2 herpesvirus subfamily. Because cellular location is frequently a determinant of regulatory function, to gain insight into additional role(s) of EBV TK and to uncover how the lymphocryptovirus and rhadinovirus enzymes differ, the subcellular localizations of EBV TK and the related cercopithecine herpesvirus-15 TK were investigated. We show that in contrast to those of the other family members, the gamma-1 herpesvirus TKs localize to the centrosome and even more precisely to the periphery of the centriole, tightly encircling the tubulin-rich centrioles in a microtubule-independent fashion. Centrosomal localization is observed in diverse cell types and occurs whether the protein is expressed independently or in the context of lytic EBV infection. Surprisingly, analysis of mutants revealed that the unique N-terminal domain was not critical for targeting to the centrosome, but rather, peptide sequences located C terminal to this domain were key. This is the first herpesvirus protein documented to reside in the centrosome, or microtubule-organizing center, an amembranous organelle that regulates the structural biology of the cell cycle through control of chromosome separation and cytokinesis. More recently, proteasome-mediated degradation of cell cycle regulatory proteins, production and loading of antigenic peptides onto HLA molecules, and transient homing of diverse virion proteins required for entry and/or egress have been shown to be coordinated at the centrosome. Potential implications of centrosomal localization for EBV TK function are discussed.
Epidermal Growth Factor Receptor Is Not Required for Human Cytomegalovirus Entry or Signaling
Authors: Isaacson Marisa K. , Feire Adam L. , Compton Teresa 
Published: April 2007

ABSTRACT
Human cytomegalovirus (HCMV) can bind, fuse, and initiate gene expression in a diverse range of vertebrate cell types. This broad cellular tropism suggests that multiple receptors and/or universally distributed receptors mediate HCMV entry. Our laboratory has recently discovered that certain β1 and β3 integrin heterodimers are critical mediators of HCMV entry into permissive fibroblasts (A. L. Feire, H. Koss, and T. Compton, Proc. Natl. Acad. Sci. USA 101:15470-15475, 2004). It has also been reported that epidermal growth factor receptor (EGFR) is necessary for HCMV-mediated signaling and entry (X. Wang, S. M. Huong, M. L. Chiu, N. Raab-Traub, and E. E. Huang, Nature 424:456-461, 2003). Integrins are known to signal synergistically with growth factor receptors, and this coordination was recently reported for EGFR and β3 integrins in the context of HCMV entry (X. Wang, D. Y. Huang, S. M. Huong, and E. S. Huang, Nat. Med. 11:515-521, 2005). However, EGFR-negative cell lines, such as hematopoietic cells, are known to be infected by HCMV. Therefore, we wished to confirm a role for EGFR in HCMV entry and then examine any interaction between β1 integrins and EGFR during the entry process. Surprisingly, we were unable to detect any role for EGFR in the process of HCMV entry into fibroblast, epithelial, or endothelial cell lines. Additionally, HCMV did not activate the EGFR kinase in fibroblast cell lines. We first examined HCMV entry into two EGFR-positive or -negative cell lines but observed no increase in entry when EGFR was expressed to high levels. Physically blocking EGFR with a neutralizing antibody in fibroblast, epithelial, or endothelial cell lines or blocking EGFR kinase signaling with a chemical inhibitor in fibroblast cells did not inhibit virus entry. Lastly, we were unable to detect phosphorylation of EGFR in fibroblasts cells in response to HCMV stimulation. Our findings demonstrate that EGFR does not play a significant role in HCMV entry or signaling. These results suggest that specific integrin heterodimers either act alone as the primary entry receptors or interact in conjunction with an additional receptor(s), other than EGFR, to facilitate virus entry.
Hepatitis B Virus X Protein Stimulates the Mitochondrial Translocation of Raf-1 via Oxidative Stress
Authors: Chen Jun , Siddiqui Aleem 
Published: April 2007

ABSTRACT

The human hepatitis B virus (HBV) X protein (HBx) plays a crucial role(s) in the viral life cycle and contributes to the onset of hepatocellular carcinoma (HCC). HBx caused the mitochondrial translocation of Raf-1 kinase either alone or in the context of whole-viral-genome transfections. Mitochondrial translocation of Raf-1 is mediated by HBx-induced oxidative stress and was dependent upon the phosphorylation of Raf-1 at the serine
338/339
and Y
340/341
residues by p21-activated protein kinase 1 and Src kinase, respectively. These studies provide an insight into the mechanisms by which HBV induces intracellular events relevant to liver disease pathogenesis, including HCC.
Characterization and Experimental Transmission of an Oncogenic Papillomavirus in Female Macaques
Authors: Wood Charles E. , Chen Zigui , Cline J. Mark , Miller Brigitte E. , Burk Robert D. 
Published: April 2007

ABSTRACT

Cervical cancer is one of the leading causes of cancer mortality in women worldwide, yet few suitable animal models currently exist for study of this disease. Virtually all cases of cervical cancer in women are caused by specific types of genital human papillomavirus (HPV). In this study, we investigated naturally occurring genital PVs in female cynomolgus macaques (
Macaca fascicularis
) without breeding contact for at least 3.5 years. Exfoliated cervicovaginal cells from 19 of 54 animals tested positive for at least one PV. Seven different PVs were identified, including four novel genotypes and two genotypes (RhPV-d and RhPV-a) previously identified in rhesus macaques (
Macaca mulatta
). Four PV types were associated with cervical intraepithelial neoplasia (CIN), which resembled human CIN by endoscopy, cervical cytology, histology, and immunohistochemistry. The presence of CIN was highly associated with PV infection (
P
< 0.0001). The most prevalent virus type was RhPV-d, which was identified in 60% of animals with CIN. An RhPV-d genome sequenced from a high-grade CIN lesion was found to be phylogenetically related to the highly oncogenic HPV16. Transfer of cervical cytobrush samples from donor animals naturally carrying RhPV-d resulted in new infections in 4 of 12 previously virus-free animals and abnormal cytology and histology in 1 of 4 infected animals after 18 weeks of infection. Experimental transmission was confirmed by E1^E4 reverse transcription-PCR products and RhPV-d sequence identity with the donor variant. These findings identify key similarities between macaque and human oncogenic PVs which should prove useful in the study of viral persistence, carcinogenesis, and therapeutic development.
Diminished Potential for B-Lymphoid Differentiation after Murine Leukemia Virus Infection In Vivo and in EML Hematopoietic Progenitor Cells
Authors: Finstad Samantha L. , Rosenberg Naomi , Levy Laura S. 
Published: April 2007

ABSTRACTInfection with a recombinant murine-feline gammaretrovirus, MoFe2, or with the parent virus, Moloney murine leukemia virus, caused significant reduction in B-lymphoid differentiation of bone marrow at 2 to 8 weeks postinfection. The suppression was selective, in that myeloid potential was significantly increased by infection. Analysis of cell surface markers and immunoglobulin H gene rearrangements in an in vitro model demonstrated normal B-lymphoid differentiation after infection but significantly reduced viability of differentiating cells. This reduction in viability may confer a selective advantage on undifferentiated lymphoid progenitors in the bone marrow of gammaretrovirus-infected animals and thereby contribute to the establishment of a premalignant state.
Human Immunodeficiency Virus Type 1 cDNAs Produced in the Presence of APOBEC3G Exhibit Defects in Plus-Strand DNA Transfer and Integration
Authors: Mbisa Jean L. , Barr Rebekah , Thomas James A. , Vandegraaff Nick , Dorweiler Irene J. , Svarovskaia Evguenia S. , Brown William L. , Mansky Louis M. , Gorelick Robert J. , Harris Reuben S. , Engelman Alan , Pathak Vinay K. 
Published: April 2007

ABSTRACT

Encapsidation of host restriction factor APOBEC3G (A3G) into
vif
-deficient human immunodeficiency virus type 1 (HIV-1) blocks virus replication at least partly by C-to-U deamination of viral minus-strand DNA, resulting in G-to-A hypermutation. A3G may also inhibit HIV-1 replication by reducing viral DNA synthesis and inducing viral DNA degradation. To gain further insight into the mechanisms of viral inhibition, we examined the metabolism of A3G-exposed viral DNA. We observed that an overall 35-fold decrease in viral infectivity was accompanied by a five- to sevenfold reduction in viral DNA synthesis. Wild-type A3G induced an additional fivefold decrease in the amount of viral DNA that was integrated into the host cell genome and similarly reduced the efficiency with which HIV-1 preintegration complexes (PICs) integrated into a target DNA in vitro. The A3G C-terminal catalytic domain was required for both of these antiviral activities. Southern blotting analysis of PICs showed that A3G reduced the efficiency and specificity of primer tRNA processing and removal, resulting in viral DNA ends that are inefficient substrates for integration and plus-strand DNA transfer. However, the decrease in plus-strand DNA transfer did not account for all of the observed decrease in viral DNA synthesis associated with A3G. These novel observations suggest that HIV-1 cDNA produced in the presence of A3G exhibits defects in primer tRNA processing, plus-strand DNA transfer, and integration.