Study on Immunopathogenesis in HIV and Hepatitis C Coinfection

Liver-related death is the leading cause of mortality in HIV-infected individuals with CD4+
cell counts over 200, and hepatitis C virus (HCV) infection is the greatest risk for
liver-related mortality in HIV-positive patients. Compared to HCV monoinfected individuals,
patients with HIV and HCV coinfection experience accelerated progression of liver fibrosis,
which can lead to higher incidence of cirrhosis, end stage liver disease (ESLD), and death.
Changes in CD8+ T-cell activation, inflammatory cytokines, and serum markers of tissue
injury may offer an immunologic platform to determine factors associated with progressive
liver fibrosis in coinfected patients. In this cross-sectional study we will evaluate
whether HIV and HCV coinfection patients with well-controlled HIV infection who have an
undetectable viral load exhibit abnormal levels of inflammation and immune activation,
potentially contributing to advanced liver fibrosis. Comparative groups include coinfected
patients successfully treated for hepatitis C, or who have absence of hepatitis C viremia
through spontaneous clearance, hepatitis C monoinfected patients, and HIV-positive patients
with well-controlled HIV infection without hepatitis C. Liver fibrosis will be measured by
non-invasive methods.

The primary objectives of this study are:

1. To determine if there are differences in markers of inflammation and immune activation
in subsets of patients with HIV, hepatitis C, and HIV and hepatitis C coinfection.

2. To assess the stage of liver fibrosis using non-invasive methods in subsets of patients
with hepatitis C and HIV and hepatitis C coinfection and compare the degree of liver
fibrosis with levels of inflammation and immune activation.