4.7 Article Proceedings Paper

Hepatitis C virus genetic variability in 52 human immunodeficiency virus-coinfected patients

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JOURNAL OF MEDICAL VIROLOGY
卷 71, 期 1, 页码 41-48

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WILEY-LISS
DOI: 10.1002/jmv.10451

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HIV-HCV coinfection; anti-HCV treatment; predictive factors; HCV variability; SSCP

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The aim of this study was to examine whether hepatitis C virus (HCV) pretreatment quasi-species complexity was linked to virological response or other clinical and biological parameters, in human immunodeficiency virus (HIV)-coinfected patients undergoing anti-HCV treatment. In addition, HCV quasispecies composition is described longitudinally in these patients before, during, and after treatment. The 52 HIV-coinfected patients were included in a randomized therapeutic trial. At inclusion, they had CD4(+) counts of >250/mul, HIV plasma load of <10,000 copies/ml, and chronic HCV infection with genotype 1 (n = 27),2 (n - 2) or 3 (n = 23). These values were compared at baseline with 32 HCV-only-infected, interferon-naive patients who were infected with genotype 1, 2, or 3 (n = 16, 1, or 15, respectively). HCV complexity was studied by single-strand conformation polymorphism (SSCP) in E2 hypervariable region 1 (HVR1), and diversity was evaluated at inclusion in 20 coinfected patients by sequencing four major SSCP bands. The baseline number of SSCP bands was identical in HIV-infected and control patients. In HIV-infected patients, HCV complexity was not predictive of sustained virological response to anti-HCV treatment and was unrelated to epidemiological factors, immunological parameters linked to HIV infection (CD4(+) counts, T CD4(+) proliferative responses to HIV-1 p24), protease inhibitor treatment, HCV plasma load, or genotype. HCV diversity was lower in genotype 2-and 3-infected patients. Six months after completion of the anti-HCV treatment, in comparison with baseline, SSCP profiles were modified in 13 of the 21 nonresponding coinfected patients with analyzable samples. In conclusion, in HIV-infected patients, HCV variability had no significant influence on virological response to anti-HCV treatment. (C) 2003 Wiley-Liss, Inc.

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