The spread of hepatitis C virus (HCV) infection is a worldwide crisis. Emerging evidence reveals the host-viral interactions govern the natural course and treatment response, individualy. For pegylated interferon plus ribavirin treatment, the response is most strongly predicted by the patient's HCV genotype. HCV genotype 1 with subtypes is the most important viral component in determining the success of direct-acting antiviral treatmenst. In addition to baseline viral load and HCV genomic heterogeneity, these two factors are linked with the treatment response. In chronic HCV infection, hosts’ genetic variations in immune responsive genes, have been identified as predictors of spontaneous disease progression and therapeutic outcome. In previous large genome-wide association studies, interferon3 gene polymorphisms have been shown to be linked with spontaneous clearance and treatment responsiveness. An inosine triphosphatase gene polymorphism has been shown to reduce the risk of anaemia and other side effects caused by the antiviral drug ribavirin. Hepatic steatosis and fibrosis are linked to a second genetic mutation in the patatin-like phospholipase domain containing 3 genes in HCV patients. This study examined the role of viral and host genetics in the natural history and treatment outcomes of HCV infection, and it is focused on the known viral and host variables linked with patient outcomes in HCV infection. This will result in fresh concepts of individualising, both the preventation to therapeutics.