Hepatology. 2009 May 6;50(1):34-45. [Epub ahead of print]

Human immunodeficiency virus and hepatitis C infections induce distinct
immunologic imprints in peripheral mononuclear cells.

Kottilil S, Yan MY, Reitano KN, Zhang X, Lempicki R, Roby G, Daucher M, Yang J,
Cortez KJ, Ghany M, Polis MA, Fauci AS.
Laboratory of Immunoregulation, National Institute of Allergy and Infectious
Diseases (NIAID), National Institutes of Health (NIH), Department of Health and
Human Services (DHHS), Bethesda, MD.


Coinfection with hepatitis C virus (HCV) is present in one-third of all human
immunodeficiency virus (HIV)-infected individuals in the United States and is
associated with rapid progression of liver fibrosis and poor response to
pegylated interferon (IFN) and ribavirin. In this study we examined gene
expression profiles in peripheral blood mononuclear cells (PBMCs) from different
groups of individuals who are monoinfected or coinfected with HIV and HCV. Data
showed that HIV and HCV viremia up-regulate genes associated with immune
activation and immunoregulatory pathways. HCV viremia is also associated with
abnormalities in all peripheral immune cells, suggesting a global effect of HCV
on the immune system. Interferon-alpha- induced genes were expressed at a higher
level in PBMCs from HIV-infected individuals. HCV and HIV infections leave
distinct profiles or gene expression of immune activation in PBMCs. HIV viremia
induces an immune activated state; by
comparison, HCV infection induces immunoregulatory and proinflammatory pathways
that may contribute to progression of liver fibrosis. Conclusion: An aberrant
type-I IFN response seen exclusively in HIV-infected individuals could be
responsible for the poor therapeutic response experienced by HIV/HCV coinfected
individuals receiving interferon-alpha- based current standard of care.
(HEPATOLOGY 2009;50:34-45. ).
PMID: 19551908 [PubMed - as supplied by publisher]


[Non-text portions of this message have been removed]