Exploration and review of the molecular mechanisms of hepatitis C virus infection-induced hepatocellular carcinoma

Laboratory medicine, STEM college, RMIT university, Melbourne, VIC 3001, Australia

^* Corresponding author: 424301687@qq.com

Abstract

Hepatitis C virus (HCV) is a virus that causes acute and chronic hepatitis, which can progress to liver damage. The link between HCV infection and hepatocellular carcinoma (HCC) has been proven by many studies. Long-term inflammation caused by HCV infection is one of the carcinogenic factors. Secondly, HCV infection significantly changes the expression of many specific genes and signaling pathways in hepatocytes. The signaling pathways affected by HCV infection have been found to be related to cellular defense mechanisms (apoptosis, proliferation, and antioxidant responses), cellular metabolism (lipid and protein metabolism), and intracellular transport (vesicles). Changes caused by HCV tend to persist and are associated with liver carcinogenesis even after cure, as evidenced by the subsequent development of HCC that persists after clearance of HCV. This study employed transcriptome sequencing data from public databases for gene enrichment analysis. The results were subsequently compared with the findings in the literature review. As a result, it was observed that HCV infection increases the risk of hepatocellular carcinoma by altering the gene expression associated with the PI3K/AKT/mTOR pathway, cellular apoptosis, protein synthesis, and intracellular transport.