The findings did not support use of pegylated interferon maintenance therapy in HCV/HIV coinfection. The SLAM-C study did identify racial disparities in HCV treatment response, with lower rates of efficacy seen in African-American and Hispanic subjects.37 The advent of new direct antivirals against HCV is eagerly awaited for HIV/HCV-coinfected patients, in whom current standard therapy with pegylated Proteasome inhibitor interferon plus ribavirin provides clearance in less than one-third of HCV genotype 1 carriers,

which unfortunately are the most prevalent.39 The new compounds for HCV, however, may face particular challenges in the coinfected population in whom the risk of drug resistance might be increased due to higher viral loads and lower activity of interferon. Furthermore, there is a high potential for interaction and interference with antiretroviral drugs due to shared cytochrome P450 metabolism profiles for many experimental agents. Despite these concerns, the U.S. Food and Drug Administration Antiviral Drug Advisory committee stipulated that studies in HCV/HIV-coinfected patients must be initiated prior to approval of

a New Drug Application in HCV-monoinfected subjects due to the significant disease burden and rapid progression observed in HCV/HIV-coinfected patients.40 Data from multiple sources suggest that only a fraction of subjects with HCV/HIV coinfection actually receive treatment for HCV. The low rate of hepatitis C therapy among HIV/HCV-coinfected patients in many U.S. cohorts,41 especially in those including veterans,42 contrasts with treatment rates of 40% in 3-Methyladenine datasheet Western Europe.43 Differences in patient population, genotype distribution (higher genotype 2 and 3 in Europe), access to medication, and perhaps variable eligibility criteria appear to account for this observation, but it seems clear that further evaluation of this disparity is warranted. About 10% of HIV patients worldwide

show persistent serum levels of hepatitis B serum antigen. The rate is higher in Southeast Asia than in Western countries. Progression to ESLD occurs faster in HIV/HBV-coinfected patients44, characteristically in the absence of significant elevated liver enzymes, because inflammatory phenomena Thymidine kinase are ameliorated in the liver of individuals with HIV, despite the paradoxically accelerated nature of fibrogenesis. There are eight HBV genotypes, each of them including multiple subtypes. Variability in HBV is constrained by the small length of the genome and overlapping of open reading frames. However, recombination and coinfection events may still challenge immune and therapeutic control of HBV.45 In contrast with lamivudine or adefovir, entecavir and tenofovir appear to show a very high genetic barrier to resistance, although entecavir use is problematic in patients with prior lamivudine exposure due to the clinical consequences of hepatitis B viral breakthrough.