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Combination antiretroviral therapy (cART) has dramatically decreased the progression to acquired immune deficiency syndrome (AIDS) and thus the human immunodeficiency virus (HIV)-related mortality in HIV-infected patients. Consequently, hepatitis C virus (HCV) has emerged as a leading cause of death in HIV/HCV co-infected patients. Pre-existing HIV infection increases the rate of chronicity in acute HCV infection1 and is associated with higher HCV viraemia.2 Most importantly, HIV/HCV co-infected patients show more rapid progression to cirrhosis and its complications.3 This particular observation is still incompletely understood and seems to contradict the assumptions that HCV by itself is not cytopathic, that the level of viraemia does not correlate with the risk of fibrosis and cirrhosis in HIV-negative patients and that liver inflammation is immune mediated.
The clinical outcome of acute hepatitis C in HIV-negative patients is associated with a strong and maintained HCV-specific CD4+ T-cell response against both structural and non-structural proteins,4 which is typically weak in patients with chronic hepatitis C. The role of HCV-specific CD4+ T-cell responses in treatment-induced viral clearance has been examined in several studies, yielding divergent results: while some studies found a moderate but significant increase in the HCV-specific CD4+ T-cell response during antiviral treatment with a peak late in the course of …
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