Molecular mechanisms of viral hepatitis induced hepatocellular carcinoma

Figure 7 Liver disease progression to hepatocellular carcinoma from chronic viral hepatitis infection. Genetics, co-morbidities, gender, age, and aflatoxin exposure influence liver disease progression along with chronic viral infection with hepatitis B, C, and/or delta virus. Cirrhosis is the greatest risk factor for development of hepatocellular carcinoma, however, hepatocellular carcinoma in the context of chronic Hepatitis B virus infection can occur in the absence of cirrhosis. Chronic hepatitis C infection can lead to steatohepatitis, which can accelerate fibrosis and cirrhosis. Superinfection with Hepatitis delta virus in individuals who have chronic Hepatitis B virus infection creates an accelerated disease course leading to liver failure and/or hepatocellular carcinoma. Many driver mutations (telomerase reverse transcriptase, TP53, CTNNB1, AXIN1, ARID1A/ARID2, NFE2L2/KEAP1/RPS6KA3, KAK1) can occur as liver disease progresses to hepatocellular carcinoma and can lead to accelerated disease progression. TERT: Telomerase reverse transcriptase; HBV: Hepatitis B virus; HDV: Hepatitis delta virus; HCV: Hepatitis C virus.