EditorialHepatitis C virus (HCV) was first discovered in the 1970s as the pathogen to cause non-A non-B hepatitis and HCV infection is the leading cause for liver transplantation and is associated with increased risk of liver fibrosis, cirrhosis and hepatocellular carcinoma [1]. With more than 185 million people having been infected with HCV worldwide, HCV infection remains a huge medical burden in most countries. Due to the limited efficacy and extensive side-effects of the standard combination therapy with pegylated interferon alpha (IFNα) and ribavirin, development of novel antivirals is urgently needed. Much progress has been made in the understanding of the HCV life cycle, including cell surface receptors that mediate virus entry, detailed mechanisms of HCV RNA replication, viral particle assembly and egress. In the meantime, HCV replicon system that allows efficient RNA replication without viral particle production and in vitro cell culture system (HCVcc) were successfully developed [2]. Coupled with the known crystal structures of HCV NS3/4A protease and RNAdependent RNA polymerase (RdRp), these new advances make the development of new direct-acting antivirals (DAAs) for HCV possible [3]. Current Standard of Care (SOC) for the Treatment of HCVAlthough there are numerous DAAs being developed in the preclinical and clinical stages, the current standard of care (SOC) for the treatment of chronic hepatitis C in most developing countries is the combination therapy with pegylated interferon alpha (PEG-IFNα) and ribavirin (RBV) [4]. With this combined treatment, sustained virological response (SVR) is achieved in 40-54% of patients infected with HCV genotype 1 and in 65-82% of patients infected with HCV genotypes 2 and 3 [5]. The efficacy of this IFN-based therapy is influenced by both viral and host factors, such as HCV RNA level at baseline, HCV genotypes, degree of liver fibrosis, and the host polymorphisms of the IL28B gene. Combination therapy with PEG-IFNα and RBV has a relatively low SVR in patients infected with HCV genotype 1 and is poorly tolerated with serious side-effects such as neutropenia, anemia, thrombocytopenia in some patients [6]. As interferon is expensive and daily injection is inconvenient, new therapy without IFN is urgently needed. Development and clinical use of DAAsBetter understanding of the virus life-cycle, especially the solution of HCV protease and polymerase structures makes the development of direct-acting antivirals (DAAs) possible. The earliest two DAAs that were approved in Europe and the United States in 2011were inhibitors of NS3/4A protease: telaprevir and boceprevir. This leads to a new therapy for HCV genotype I-triple therapy (telaprevir or boceprevir in combination with pegIFN and RBV). It has been shown that this triple therapy is more effective than pegIFN and RBV combination regimen with a significant increase of SVR to 75% of patients chronically infected with HCV genotype1 [7]. Different groups of people respond to triple therapy very differently. This therapy fai...