ABSTRACT
It is known that patients with hepatitis C virus (HCV) infection that has progressed to cirrhosis are at high risk for decompensated liver disease, hepatocellular carcinoma (HCC), and possible need for liver transplant. Treatment of HCV with curative therapies reduces these risks and can improve liver function. There are at least seven different HCV genotypes with significant variation across geographic regions (Smith et al., 2014). Globally, genotype 1 (GT-1) accounts for 46% of all patients infected with HCV, followed by GT-3 (22%), and finally GT-2 and GT-4 (13% each) (Gower et al., 2014). GT-1b accounts for 22% of all infections globally (Gower et al., 2014). HCV GT-1 infection is seen most commonly in North America, Australasia, Europe, and Latin America (53–71% of all cases), GT-3 accounts for 40% of all infections in Asia, GT-4 infection is most common in the Middle East as well as in North and sub-Saharan Africa (71%), and GT-5 and GT-6 are most common in South Africa and Southeast Asia, respectively (Gower et al., 2014). Pegylated interferon (PEG-IFN) therapies with or without ribavirin (RBV) have been relatively inefficacious in curing HCV infections in GT-1 and GT-4 patients and are poorly tolerated with significant side effects. The sustained virologic response rates at 24 weeks (SVR24) (i.e. the proportion of patients whose plasma HIV RNA are undetectable 24 weeks after cessation of therapy) in patients with HCV infection receiving 48 weeks of PEG-IFN plus RBV reached 40–50% in GT-1 patients and between 50% and 79% in GT-4 patients (McHutchison et al., 2009; Kamal et al., 2008).
