Host Versus Virus: The Genetics in HCV Infection Leading to Treatment

Abstract

The spread of hepatitis C virus (HCV) infection is a worldwide crisis. Intricate host-viral interactions control the HCV infection’s natural course and treatment response according to new research. The patient’s HCV genotype is the best predictor of response to pegylated interferon plus ribavirin therapy. The most crucial viral factor in determining the efficacy of direct-acting antiviral therapy is the HCV genotype 1 subtype. In addition to baseline viral load and HCV genomic heterogeneity, these two factors are linked with the treatment response. 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. In HCV patients, a second genetic mutation in the three-gene patatin-like phospholipase domain is associated with hepatic steatosis and fibrosis. This study examined the effects of viral and host genetics on the course and results of HCV therapy while concentrating on the known viral and host variables linked to HCV patient outcomes. This will result in fresh concepts for individualising both preventative care and therapeutic treatment.