AIDS 2002: HIV Linked to Pathogenesis of Hepatitis C-Related Fibrosis
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AIDS 2002: HIV Linked to Pathogenesis of Hepatitis C-Related Fibrosis

By Michael Smith
Special to DG News

BARCELONA, SPAIN -- July 12, 2002 -- HIV viral load is significantly correlated with the development of hepatitis C-related fibrosis, suggesting a direct role for HIV in hepatitis pathogenesis, researchers said at the 14th International AIDS Conference.

Eighty percent of individuals infected with the hepatitis C virus (HCV) develop chronic infection, and up to 20 percent will eventually develop cirrhosis. Co-infection with HIV is common, but the factors that correlate with pathogenesis in co-infected individuals have not been determined.

According to Kathleen Stellrecht, MD, of Albany Medical Center, in Albany, New York, United States, HIV viral load but -- not HCV viral load or HCV genotype -- significantly correlates with hepatitis disease progression.

Dr. Stellrecht and colleagues performed a retrospective analysis of 28 HIV- and HCV-infected patients, of whom 75 percent were male. Their mean CD4 count was 363 cells/mm3 of blood, and their mean HIV and HCV loads were 4.36 and 6.52 log viral copies/mL, respectively.

The patients’ mean alanine transaminase level (ALT) was 87, with a range from 22 to 191. Their mean fibrosis score was 0.9, with a range from one to four, and their mean Knodell score was 6.92, with a range of two to 14.

The univariate statistical analysis carried out by the researchers showed that ALT levels, levels of aspartate aminotransferase (AST), and HIV viral loads were all significantly correlated with the risk of developing fibrosis. However, a multivariate analysis revealed that AST and ALT were not independent predictors of the development of fibrosis, leaving increasing HIV viral load as the only independent risk factor associated with liver disease, in terms of Knodell score and fibrosis score.

The findings suggest a direct role for HIV in the progression of HCV, Dr. Stellrecht said, adding that their work supports the need to keep viral loads low in order to minimize the progression of the HCV.

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