Affiliation: | aPublic Health Department, Generalitat Valenciana and Evolutionary Genetics Unit, Institut Cavanilles de Biodiversitat i Biologia Evolutiva, University of Valencia, Apt. Of. 2085, E-46071 Valencia, Spain bCIBER-ESP (Network Center for Biomedical Research in Epidemiology and Public Health), Spain cCentre for Liver Disease & Transplant, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, United States dGI unit, San Francisco Veterans Administration Medical Center 111B and Department of Medicine, University of California San Francisco, 4150 Clement Street, San Francisco, CA 94121, USA eHepatogastroenterology Service, Hospital Universitari La Fe, Av. Campanar 21, 46009 Valencia, Spain fCIBER-EHD (Network Center for Biomedical Research in Hepatic and Digestive Diseases), Spain |
Abstract: | Chronic infection by Hepatitis C Virus (HCV) causes liver fibrosis, which is accelerated by unknown mechanisms in patients with HIV-1 coinfection. The evolution of HCV quasispecies in this setting of coinfection is not fully understood. To compare HCV quasispecies between HIV–HCV coinfection and HCV monoinfection, we sequenced 340 HCV clones from the HVR-1 and NS3 regions at two different time points in two groups of treatment-naïve patients with HCV-1a infection: (1) HIV–HCV positive (n = 6); and (2) HIV negative–HCV positive (n = 3). In HCV/HIV coinfection, we found a trend for reduced HCV genetic complexity and diversity, and a trend towards reduced dN/dS ratios in the HVR-1 region, especially in those patients with CD4 < 200 cells/mm3, who lost positive selective immune pressure in the HVR-1 region. Differences in immune regulation of HCV quasispecies in HIV coinfected individuals deserve further exploration to clarify the different outcomes of chronic hepatitis C noted between the immunocompromised and the immunocompetent host. |