Highlights of the Third International Workshop on HIV and Hepatitis Coinfection

Abstract

Apart from a highly productive lifecycle, HCV is genetically highly diverse, far more so than HIV-1 and HBV. Quasi species rapidly evolve after infection with HCV. This evolution is driven by the host HLA-system and by antiHCV drugs, but also by functional constraints in terms of reversion of sequences towards consensus. Ray presented interesting data demonstrating that evolution of the virus occurs rapidly within weeks after infection. Over the course of years to decades, his group has demonstrated that within a particular host the virus may evolve to genetically distinct subtypes. Recently, another mechanism of genetic diversification, not previously described for HCV, has been discovered. Ray presented data on the recombination of two different HCVs, which may confound genotyping and lead to rapid evolution of drug resistance. The high variability of HCV clearly suggests that future drug therapy with HCV-polymerase and protease inhibitors will have to take into account the rapid evolution of drug resistance. Combination therapy as currently approached, for instance by telaprevir, which is tested together with concomitant pegylated interferon/ribavirin combination therapy, will probably be the only way to circumvent the issue of the rapid evolution of drug resistance.