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It is estimated that up to a third of the world’s HIV-infected population is co-infected with hepatitis C (HCV).1 Liver disease contributes significantly to overall morbidity and mortality in HIV-infected individuals.2 The interaction between these two viruses appears to be unidirectional. There is now ample data describing increased risk of hepatic fibrosis progression and faster progression to end-stage liver disease in HIV/HCV co-infected patients compared to HCV mono-infected patients.3 On the other hand there seems to be little effect of HCV on HIV-related progression of immune suppression or response to combination antiretroviral therapies (cART).4 Although, pegylated-interferon alpha and ribavirin combination therapy are standard of care for HCV treatment in this group of patients, sustained viral clearance rates are much lower than those seen in mono-infected patients.5 There is therefore an urgent need to understand and perhaps modify factors that may contribute to fibrosis progression whilst we await the arrival of more effective specifically-targeted antiviral therapies.
HIV-related immune suppression has a profound and complex effect on HCV-associated hepatic inflammation and fibrosis.6 This causes immune dysregulation in response to HCV that in turn promotes inflammation and fibrosis and is also associated with very high HCV viral loads. Furthermore, HIV may have direct or indirect effects on hepatic stallete cells leading to activation and promotion of fibrogenesis.7 Intuitively, cART-related suppression of HIV replication and reversal of immune suppression would thus be expected to slow down fibrosis progression and ultimately the risk of progression to end-stage liver disease. Although studies in the early cART era suggested a beneficial effect …