JOURNAL ARTICLE
MULTICENTER STUDY

Coinfection with hepatitis viruses and outcome of initial antiretroviral regimens in previously naive HIV-infected subjects

Andrea De Luca, Roberto Bugarini, Alessandro Cozzi Lepri, Massimo Puoti, Enrico Girardi, Andrea Antinori, Antonio Poggio, Gabriella Pagano, Giulia Tositti, Gianpiero Cadeo, Antonio Macor, Mario Toti, Antonella D'Arminio Monforte et al.
Archives of Internal Medicine 2002 October 14, 162 (18): 2125-32
12374521

BACKGROUND: The effect of chronic coinfection with hepatitis viruses on the response to therapy against human immunodeficiency virus 1 (HIV-1) remains debated.

METHODS: In a prospective cohort study, the effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) serostatus on the outcome of potent HIV-1 therapy was analyzed in HIV-1-infected patients previously naive to antiretroviral therapy. Changes from baseline CD4+ cell counts and HIV RNA levels over time were analyzed by linear regression models. Time to clinical progression and time to reach virologic and immunologic response were analyzed by multivariate Cox proportional hazards regression models.

RESULTS: We studied 1320 patients, among whom 600 were HCV antibody-positive and 90 were HBV surface antigen-positive. During a median follow-up of 37 months (range, 1-48 months), clinical progression was observed in 99 patients (56 new acquired immunodeficiency syndrome-defining events and 43 deaths). In multivariate models, HCV-positive HBV-negative patients showed a shorter time to clinical progression (hazard ratio, 1.55; 95% confidence interval, 1.00-2.41). Patients who were HCV-positive also showed mean CD4+ recoveries over time that were at least 30 cells/ micro L fewer than those of seronegative patients. Hepatitis virus serostatus did not affect the virologic response to HIV-1 therapy.

CONCLUSIONS: Clinical progression of HIV-1 disease after starting potent antiretroviral therapy is accelerated by concomitant infection with HCV. Compared with patients without coinfection, coinfected patients showed impaired CD4+ cell recovery, despite similar virologic response to HIV-1 therapy. These findings may have important implications for the treatment of HCV and for the timing of initiation of HIV-1 therapy in coinfected individuals.

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