Journal Article

Role of Hepatitis C Virus (HCV) Viremia and HCV Genotype in the Immune Recovery from Highly Active Antiretroviral Therapy in a Cohort of Antiretroviral-Naive HIV-Infected Individuals

Giorgio Antonucci, Enrico Girardi, Alessandro Cozzi-Lepri, Maria Rosaria Capobianchi, Andrea De Luca, Massimo Puoti, Enzo Petrelli, Giuseppe Carnevale, Giuliano Rizzardini, Paolo Antonio Grossi, Paolo Viganý, Maria Cristina Moioli, Fabrizio Carletti, Mariacarmela Solmone, Giuseppe Ippolito and Antonella D'Arminio Monforte

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 40, issue 12, pages e101-e109
Published in print June 2005 | ISSN: 1058-4838
Published online June 2005 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/430445
Role of Hepatitis C Virus (HCV) Viremia and HCV Genotype in the Immune Recovery from Highly Active Antiretroviral Therapy in a Cohort of Antiretroviral-Naive HIV-Infected Individuals

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Background. The roles of hepatitis C virus (HCV) viremia and HCV genotype in the immune response to highly active antiretroviral therapy (HAART) are poorly understood. Our aim was to assess the CD4+ cell count recovery after HAART in human immunodeficiency virus (HIV)–infected patients with HCV viremia and HIV-infected patients who tested negative for HCV antibody (HCV-Ab). We also aimed to assess whether the response to HAART in these patients varied according to HCV genotype.

Methods. The analysis focused on 1219 HCV-Ab—negative patients and 284 HCV-viremic patients from a cohort of HIV-infected subjects that includes persons who were antiretroviral naive before initiating HAART after cohort enrollment. HCV RNA load and HCV genotype were determined in plasma specimens obtained and stored during the 6-month period preceding the initiation of HAART.

Results. The chance of achieving a CD4+ cell count increase of ⩾100 cells/µL from the pre-HAART level tended to be poorer in HCV-viremic patients than in patients who tested negative for HCV-Ab (adjusted relative hazard [RH], 0.82; 95% confidence interval [CI], 0.66–1.01;P = .06). In contrast, a comparison of patients who had a HCV RNA load >1 × 106 IU/mL with patients who had a HCV RNA load of 5–1 × 106 IU/mL revealed no significant association between HCV RNA load and achievement of an increased CD4+ cell count (adjusted RH, 0.97; 95% CI, 0.75–1.27;P = .83). There was no clear association between HCV genotype and the probability of achieving a CD4+ cell count increase.

Conclusions. An association between the presence of HCV-Ab and immune reconstitution after HAART has been shown elsewhere. Results of our large, prospective study support a direct role of HCV viremia in the CD4+ cell count response to HAART. Moreover, our results underline the fact that, in individuals coinfected with HIV and HCV, the goal of treating HCV infection is to eradicate HCV, to both slow the rate of HCV progression and limit potential interference with the response to HAART.

Journal Article.  5238 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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