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Chronic hepatitis C virus (HCV) infection can cause fibrosis and may accelerate the course of HIV infection. We conducted a cross-sectional study of HIV-HCV coinfected patients receiving highly active antiretroviral therapy to determine the effects of treatment on HIV load, HCV RNA, and fibrosis. Patients coinfected with HIV and HCV (n = 37) without a previous treatment with HCV-specific nucleoside analogues were included. The median age was 50 years, and the median duration of HCV infection was 14 years. The median number of CD4+ T lymphocytes was 528 per microL, and the median HIV load was less than the limit of quantification (0.03 IU/mL). Mean liver stiffness was 7.5 kPa. Forty-one percent of patients were taking nucleoside analogues; hepatitis B virus (HBV) therapy was given to 29% of patients, and HCV therapy to 20%. Eight (22%) patients had an HIV load less than 200 copies per milliliter, and 3 of these patients had an undetectable load. HCV load was high in all patients with a suppressed HIV load. No statistically significant difference in HCV load was observed between patients with an HIV load greater than or equal to 100 copies per milliliter and those with a suppressed HIV load. Charts of 50 patients indicated no effect of therapy on HCV load or liver stiffness; however, more data are needed to confirm the absence of change in these parameters. Hepatitis C virus load was not lower in patients with HIV loads less than 100 copies per milliliter than in those with greater than 100 copies per milliliter (median, 5.09 vs. 4.91 log10 copies per milliliter, respectively; P = 0.935). Nine patients had a > or =0.5-fold decrease in liver stiffness; 2 (29%) of the patients with a HIV load less than 200 copies per milliliter had a greater than or equal to 0.5-fold decrease in liver stiffness compared with none
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