title: Stronger hepatitis C virus-specific CD8+ T-cell responses in HIV coinfection.
abstract: Hepatitis C virus (HCV) is a widespread chronic infection that shares routes of transmission with human immunodeficiency virus (HIV). Thus, coinfection with these viruses is a relatively common and growing problem. In general, liver disease develops over years with HIV coinfection, when compared to decades in HCV monoinfection. The role of the immune system in the accelerated pathogenesis of liver disease in HIV/HCV coinfection is not clear. In this study, we compared the frequency, magnitude, breadth and specificity of peripheral blood CD4+ and CD8+ T-cell responses between HCV-monoinfected and HCV/HIV-coinfected individuals and between HIV/HCV-coinfected subgroups distinguished by anti-HCV antibody and HCV RNA status. While HIV coinfection tended to reduce the frequency and breadth of anti-HCV CD8+ T-cell responses in general, responses that were present were substantially stronger than in monoinfection. In all groups, HCV-specific CD4+ T-cell responses were rare and weak, independent of either nadir or concurrent CD4+ T-cell counts of HIV-infected individuals. Subgroup analysis demonstrated restricted breadth of CD8+ HCV-specific T-cell responses and lower B-cell counts in HIV/HCV-coinfected individuals without anti-HCV antibodies. The greatest difference between HIV/HCV-coinfected and HCV-monoinfected groups was substantially stronger HCV-specific CD8+ T-cell responses in the HIV-coinfected group, which may relate to accelerated liver disease in this setting.
authors.affiliation: Immunology Program, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada. lisa.barrett@dal.ca
authors.forename: L
authors.initials: L
authors.lastname: Barrett
authors.forename: M
authors.initials: M
authors.lastname: Gallant
authors.forename: C
authors.initials: C
authors.lastname: Howley
authors.forename: M
authors.initials: M
authors.lastname: Ian Bowmer
authors.forename: G
authors.initials: G
authors.lastname: Hirsch
authors.forename: K
authors.initials: K
authors.lastname: Peltekian
authors.forename: M
authors.initials: M
authors.lastname: Grant
mesh_terms: D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D048708:Cell Growth Processes / Q000276:immunology; D015331:Cohort Studies; D005260:Female; D006678:HIV / Q000276:immunology*; D015658:HIV Infections / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000821:virology; D016174:Hepacivirus / Q000276:immunology*; D018937:Hepatitis C Antibodies / Q000097:blood; D019698:Hepatitis C, Chronic / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000821:virology; D006801:Humans; D007371:Interferon-gamma / Q000097:blood; D008297:Male; D008875:Middle Aged; D018709:Statistics, Nonparametric
chemical_list: D018937:Hepatitis C Antibodies; D007371:Interferon-gamma