Abstract
Chronic hepatitis C virus (HCV) coinfects nearly 25% of HIV patients and it has been associated with more rapid progression of liver fibrosis, leading to cirrhosis, end-stage liver disease and hepatocellular carcinoma.
Emerging data support multiple derangements attending HIV coinfection, including increases in profibrogenic cytokine expression and secretion, generation of enhanced oxidative stress, and increases in hepatocyte apoptosis. Furthermore, liver-related death is a major cause of morbidity and mortality in HCV/HIV coinfected patients on antiretroviral therapy therefore, anti-HCV treatment is advised to be considered for all HCV/HIV patients. Unfortunately, treatment with pegylated interferon (PegIFN) plus ribavirin (RBV) has shown a low efficacy in these patients, mainly among those coinfected with genotype 1. Triple therapy with PegIFN plus RBV and telaprevir or boceprevir, the first approved direct-acting antiviral agents (DAAs) will improve the likelihood of cure for genotype 1 infected patients. Nevertheless, a significant number of coinfected patients are ineligible for IFN-containing regimens and concerns remain in regard with drug-to-drug interactions and safety of triple therapy in cirrhotic patients.
Furthermore, therapeutic decisions today need take into account the promise of new DAAs, some combined in IFN-free regimens, currently being investigated in multiple clinical trials to be in a near future, an easier, shorter and more effective HCV treatment in HIV coinfected patients.
Keywords: Direct antiviral-acting agents, HCV/HIV coinfection, immunobiology, liver fibrosis, PegInterferon, treatment.
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