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• W2063993043 abstract "Chronic hepatitis C is common among HIV-infected patients who acquired the infection through contaminated blood exposure, such as intravenous drugs users (IDU) or haemophiliacs [1]. Liver disease seems to progress faster to cirrhosis in this population [2,3], and recent data have underlined both a higher risk of hepatotoxicity using antiretroviral drugs in HIV-positive individuals carrying hepatitis C virus (HCV) [4], and an increasing morbidity and mortality secondary to end-stage liver disease in this population [5]. On average, HIV-infected patients harbour 10-fold higher titres of HCV viraemia compared with HIV-negative persons, which could be explained by the immunosuppression operated by HIV. In this context, we have examined the impact of highly active antiretroviral therapy (HAART) on HCV replication. In a previous report [6], we could not demonstrate reductions in HCV viraemia shortly after beginning HAART, even in patients experiencing both a dramatic immunological restoration and a rapid plasma HIV clearance. Similar results have been found by other authors [7,8], and in one study [9], HCV viraemia even increased transiently after the initiation of HAART. In contrast, Fialaire et al. [10] reported a sustained disappearance of HCV in the blood of patients experiencing a good response to HAART. In order to elucidate whether immune reconstitution after HAART can diminish HCV replication, we analysed 16 subjects co-infected with HIV and HCV who reached undetectable plasma viraemia after beginning a triple combination with two nucleoside analogues and one protease inhibitor. HIV RNA was measured using the third-generation bDNA assay (Bayer Diagnostics, Barcelona, Spain), which has a detection limit of 50 HIV-RNA copies/ml [11]. With respect to HCV RNA, quantification was performed using a commercially available reverse transcriptase–polymerase chain reaction assay (COBAS Amplicor, Roche Diagnostics, Barcelona, Spain), which has a detection limit of 100–1000 HCV RNA copies/ml [12]. Samples collected at baseline, and after 3 and 12 months on HAART were analysed. The mean HCV load at baseline was approximately 107 HCV RNA copies/ml. It remained without a significant change at 3 months, but declined to levels below 106 copies/ml after 12 months of successful antiretroviral treatment. The mean increase in the CD4 cell count was 210 ± 18 cells/μl at 12 months. Overall, seven out of 16 patients (43.7%) showed a decline in HCV titre above 0.5 log at 12 months on HAART, and in four (23.5%) HCV viraemia became undetectable. Our results support the theory that the high levels of HCV viraemia seen in HIV co-infected individuals are secondary to the immunosuppression caused by HIV itself, and that immune reconstitution occurring after the introduction of antiretroviral therapy leads to the control of HCV replication only after a prolonged period of HIV suppression. Whether this effect is translated into an amelioration of the course of liver disease in co-infected individuals needs to be examined further. Mayte Pérez-Olmedaa Javier García-Samaniegob Vincent Sorianoa" @default.
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• W2063993043 date "2000-01-01" @default.
• W2063993043 modified "2023-09-22" @default.
• W2063993043 title "Hepatitis C viraemia in HIV–HCV co-infected patients having immune restoration with highly active antiretroviral therapy" @default.
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• W2063993043 doi "https://doi.org/10.1097/00002030-200001280-00023" @default.
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