Immunopathogenesis of hepatitis C virus in the immunosuppressed host


Dr. Margaret Koziel
Harvard Institutes of  Medicine
Room 223a
Beth Israel Deaconess Medical Center
330 Brookline Ave
Boston MA, 02215
Tel: 617 667 0038
Fax: 617 975 5235
e-mail: mkoziel@caregroup.harvard. edu


The prevalence of chronic hepatitis C virus (HCV) infection among various groups of immunosuppressed patients is high. These groups include patients co-infected with human immunodeficiency virus (HIV), recipients of organ transplants, and those with hypogammaglobulinemia. The liver disease in the immunosuppressed host is typically severe with an unusually rapid progression to cirrhosis. This is somewhat paradoxical, as the classical model for HCV-induced liver disease assumes that cell-mediated immune responses induce liver injury. It is likely that a combination of viral-related factors and host-related factors plays a role in this accelerated natural history of HCV. Data are accumulating in immunocompromised hosts that address the immunopathogenesis of liver injury, although there are still fundamental gaps in our understanding of this process. In this review, we will focus on our current understanding of the mechanisms of liver injury and how it relates to the accelerated liver disease progression in immunocompromised hosts.