title: Hepatitis C virus replication in Caucasian HIV controllers.
abstract: Whether HIV controllers, patients who spontaneously control HIV viraemia, are able to control hepatitis C virus (HCV) infection, in terms of spontaneous clearance or lower HCV replication, is not well understood. To assess to what extent Caucasian HIV controllers are able to control HCV replication and potential associated factors, plasma HIV-1 and HCV RNA levels, anti-HCV antibodies, HCV genotype and human leucocyte antigens (HLA) typing were determined in samples from 75 HIV controllers (33 viraemic controllers, <1000 HIV-1 RNA copies/mL, and 42 elite controllers, <40 HIV-1 RNA copies/mL) and compared with 261 HIV-infected noncontrollers. We did not find differences in the HCV spontaneous clearance rates between groups. However, we interestingly found a lower HCV viral load in HIV controllers, alongside a different distribution of HCV genotypes in relation to the comparison group. In addition, HLA-B57 was associated with a lower HCV viral load in the control group and HIV controllers, and conversely, HLA-B35 with higher HCV viral load in HIV controllers. The subrepresentation of HCV genotype 1 and the overrepresentation of HLA-B57 only partly explained the lower HCV viral load found in HIV controllers. In fact, HIV controller status was independently associated with lower HCV viral load, together with HCV genotype non-1, the presence of HLA-B57 and absence of HLA-B35. Caucasian HIV controllers are able to better control HCV replication, in terms of lower HCV viral load levels. These findings support the idea that some common host mechanisms are involved in the defence against these two persistent infections.
authors.affiliation: Immunovirology Laboratory and Biochemistry Department, Infectious Diseases Service, Virgen del Rocio University Hospital/Biomedicine Institute of Seville (IBIS), Avd. Manuel Siurot s/n, Seville Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain.
authors.forename: E
authors.initials: E
authors.lastname: Ruiz-Mateos
authors.forename: K
authors.initials: K
authors.lastname: Machmach
authors.forename: M C
authors.initials: MC
authors.lastname: Romero-Sanchez
authors.forename: S
authors.initials: S
authors.lastname: Ferrando-Martinez
authors.forename: P
authors.initials: P
authors.lastname: Viciana
authors.forename: M
authors.initials: M
authors.lastname: Del Val
authors.forename: M A
authors.initials: MA
authors.lastname: Muñoz-Fernandez
authors.forename: M
authors.initials: M
authors.lastname: Genebat
authors.forename: M
authors.initials: M
authors.lastname: Leal
mesh_terms: D000328:Adult; D060085:Coinfection / Q000821:virology*; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000276:immunology / Q000821:virology; D015235:HLA-B Antigens / Q000276:immunology; D015797:HLA-B35 Antigen / Q000276:immunology; D016174:Hepacivirus / Q000502:physiology*; D006526:Hepatitis C / Q000150:complications / Q000276:immunology / Q000821:virology*; D006801:Humans; D007113:Immunity, Innate; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000096:biosynthesis / Q000097:blood / Q000276:immunology; D019562:Viral Load; D014766:Viremia / Q000276:immunology / Q000821:virology; D014779:Virus Replication; D044465:White People
chemical_list: D015235:HLA-B Antigens; D015797:HLA-B35 Antigen; C103707:HLA-B57 antigen; D012367:RNA, Viral