These patients should be referred to Hepatology units working with a liver transplantation programme. Factors which are associated with a reduced chance of achieving SVR include a high pretreatment HCV viral titre, failure to achieve RVR or http://www.selleckchem.com/products/BIBW2992.html EVR, genotype 1 infection, presence of cirrhosis, older age at the time of infection and African racial origin. A genetic polymorphism near the IL28B gene encoding for interferon-λ-3 has been identified as being associated with a twofold difference in response to PegIFN/ribavirin treatment [12]. Testing for the IL28B polymorphism can now be performed in most hepatology reference

centres and can provide useful information to decide which treatment regimen to start. HCV RNA should be assessed in all HIV-positive persons, as approximately 6% of these individuals fail to develop detectable HCV antibodies so a negative antibody test result should not be interpreted as indicating that the patient does not have HCV infection. The management of these patients has been reviewed recently in the UKHCDO guidelines

[10]. Patients coinfected with HIV and HCV have an approximately twofold greater risk of developing cirrhosis, and progress more rapidly to liver failure compared with HCV anti-CTLA-4 antibody monoinfected individuals. The importance of the need to treat HCV in this patient group should therefore be emphasized. To optimize

response to anti-HCV treatment, HIV infection should be fully suppressed using HAART. HAART regimens should not include zidovudine (AZT) as this is contraindicated with ribavirin because of the potential for severe anaemia. Didanosine and stavudine should also be avoided because of the interaction with ribavirin and the risk of potentially fatal lactic acidosis. The impact of abacavir on treatment responses to HCV combination therapy is currently debated. HIV non-progressors who are maintaining normal CD4 counts, not on HAART should also be encouraged to undertake HCV treatment. Co-infected patients have lower SVRs with PegIFN/ribavirin treatment compared with 上海皓元医药股份有限公司 monoinfected individuals. In the meta-analysis reported by Franchini, coinfected patients had an overall SVR of 29% [9]. Clinical trials of protease inhibitor based triple therapy are currently ongoing in HIV/HCV coinfected patients to assess, safety and efficacy, as well as drug–drug interactions which can be problematic in this patient population. The first direct acting antivirals belonging to the class of protease inhibitors (boceprevir, telaprevir) have been recently approved, but are restricted to the treatment of HCV genotype 1 infections [13].