Background: Although there is clear evidence of an accelerated progression of liver fibrosis in HIV-positive patients with chronic hepatitis C virus (HCV) infection, it is unclear whether HCV infection may influence HIV-1 disease progression. We have analyzed the impact of HCV on CD4 counts and plasma HIV RNA in a large group of HIV-positive individuals.
Method: Epidemiological data, CD4 counts, and plasma HIV RNA values were recorded from 902 consecutive HIV-1-positive persons who attended our institution since 1998.
Results: HCV infection was documented (antibodies and/or HCV RNA) in 72% of the total study population. The higher rates were seen among intravenous drug users (97%) compared to other groups (17% in homosexual men, 23% in patients who acquired HIV heterosexually). In a cross-sectional analysis performed at the first trimester of 2000, the mean CD4 count was lower among HCV-positive than among HCV-negative individuals (518 +/- 282 cells/microL vs. 620 +/- 302 cells/microL; p <.001). The mean plasma HIV RNA was 11,188 +/- 55,301 copies/mL in HCV-positive persons versus 6,352 +/- 32,152 copies/mL in HCV-negative persons (p =.03). Undetectable plasma HIV RNA (<50 copies/mL) was recognized in 54% of HCV-positive persons versus 64% of HCV negative persons (p =.04); a similar proportion of patients in each group was on antiretroviral therapy (90% vs. 93%) or HAART (86% vs. 89%). When comparing data from 1998 and 2000, the CD4 count increased an average of 53 cells/microL (11%) in HCV-positive persons versus 111 (19%) in HIV-negative persons during this 2-year interval (p <.05). Plasma HIV RNA on average declined 606 copies/mL (5%) in HCV-positive persons versus 5,788 copies/mL (54%) in HCV-negative persons (p <.05). A significant association between HCV infection and CD4 counts was recognized in the multivariate analysis, which was independent of gender, age, plasma HIV RNA, use of HAART, and adherence to therapy. In contrast, no significant effect of HCV on HIV RNA was found.
Conclusion: Hepatitis C may be associated with a poor immunologic outcome in HIV-infected persons. This worst influence is not explained by a lower rate of antiretroviral therapy among HCV-positive persons nor a much poorer drug adherence in this population. Therefore, hepatitis C may act as a direct cofactor for HIV disease progression. If so, treatment of chronic hepatitis C might indirectly benefit HIV disease.