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Liver disease has become the second most common cause of death of HIV-infected patients,1 and the risk of liver-related death increases with progressive HIV-associated immunodeficiency.2 This observation allows for the possibility that the pathogenic mechanisms which promote T cell depletion may also promote liver injury. In HIV-infected patients, liver disease occurs most commonly from hepatitis C virus (HCV) co-infection, active hepatitis B virus (HBV) infection, non-alcoholic steatohepatitis (NASH)3 as well as alcohol-associated steatohepatitis.4
However, due to common modes of transmission, HCV infection is the most frequent cause of liver disease found in HIV-infected persons. It has been shown that the overall prevalence of HCV infection among HIV-infected individuals is ∼30–50%, with rates of co-infection as high as 90% in intravenous drug users and almost 100% in haemophiliacs.5
To date it is known that the HIV genome encodes structural, regulatory and accessory proteins: the 160 kDa Env protein (gp160) is cleaved by cellular proteases to generate gp41 and gp120.6 In turn, gp120 envelope protein, expressed in tissue, on the surface of virions or even as a free protein, may act on specific target cells. However, it is still unclear whether and how gp120 may interfere with fibrosis acting on hepatic stellate cells (HSCs), one of the subpopulation involved in …
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