title: Hepatitis C virus genetic variability in 52 human immunodeficiency virus-coinfected patients.
abstract: The aim of this study was to examine whether hepatitis C virus (HCV) pretreatment quasispecies 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/micro l, 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.
authors.affiliation: Virology Laboratory, University of Victor Segalen, Bordeaux, France. didier.neau@chu-bordeaux.fr
authors.forename: Didier
authors.initials: D
authors.lastname: Neau
authors.forename: Anne-Christine
authors.initials: AC
authors.lastname: Jouvencel
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Legrand
authors.forename: Pascale
authors.initials: P
authors.lastname: Trimoulet
authors.forename: Tatiana
authors.initials: T
authors.lastname: Galperine
authors.forename: Isabelle
authors.initials: I
authors.lastname: Chitty
authors.forename: Michel
authors.initials: M
authors.lastname: Ventura
authors.forename: Brigitte
authors.initials: B
authors.lastname: Le Bail
authors.forename: Philippe
authors.initials: P
authors.lastname: Morlat
authors.forename: Jean-Yves
authors.initials: JY
authors.lastname: Lacut
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Ragnaud
authors.forename: Michel
authors.initials: M
authors.lastname: Dupon
authors.forename: Hervé
authors.initials: H
authors.lastname: Fleury
authors.forename: Marie-Edith
authors.initials: ME
authors.lastname: Lafon
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000188:drug therapy / Q000821:virology; D000293:Adolescent; D000328:Adult; D005260:Female; D014644:Genetic Variation / Q000235:genetics*; D005838:Genotype; D015658:HIV Infections / Q000150:complications*; D016174:Hepacivirus / Q000235:genetics* / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy / Q000821:virology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018807:Polymorphism, Single-Stranded Conformational