AMB Volume 40, Issue 3, 2024 Pages 277-289 https://doi.org/10.59393/amb24400301
Chronic Viral Infections and Hepatic Oncogenesis
Alexandrova R., Hristov H., Kirov P., Abudalleh A., Zhivkova T., Dyakova L., Dimitrov G.
Hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis D virus (HDV) are major contributors to chronic liver disease and hepatocellular carcinoma (HCC) worldwide. Discovered in the 1960s and 1980s, these viruses are associated with significant global health burdens. HBV, a member of the Hepadnaviridae family, is a partially double-stranded DNA virus responsible for chronic liver infections that can lead to HCC. Despite the success of HBV vaccination, challenges such as vaccine escape mutants and non-responders persist. HCV, a member of the Flaviviridae family and a positive-sense single-stranded RNA virus, affects millions globally. While direct-acting antivirals (DAAs) can achieve high rates of viral clearance, vaccine development remains hindered by genetic diversity and immune evasion. HDV, the smallest known human virus, relies on HBV for its propagation. It exacerbates liver disease and increases HCC risk, particularly in co-infected individuals. HDV does not integrate into the host genome, suggesting indirect mechanisms of carcinogenesis, potentially through interactions with HBV. Addressing these challenges requires enhanced vaccination strategies, improved antiviral therapies, and continued research to understand the complex interplay between these viruses and liver cancer development.
Keywords: virus-induced oncogenesis, hepatocellular carcinoma, hepatitis viruses, antiviral treatment, vaccines
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