Cancer is a multifactorial disease driven by genetic, epigenetic, and environmental factors, including biological agents such as oncogenic viruses. Among these, hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis D virus (HDV) play a significant role in the pathogenesis of hepatocellular carcinoma (HCC), the most common form of primary liver cancer and a major contributor to global cancer mortality. Chronic infections with these viruses induce liver carcinogenesis through a combination of direct mechanisms—such as viral genome integration and oncoprotein expression and indirect pathways involving persistent inflammation, immune evasion, and oxidative stress. Despite advancements in HBV vaccination and curative therapies for HCV, the global burden of hepatitis-related liver cancer remains substantial due to underdiagnosis, limited access to care, and the absence of a functional cure for HBV. This review critically explores the molecular biology of HBV, HCV, and HDV, their roles in cancer initiation and progression, and current therapeutic strategies. It also highlights emerging research directions essential for improving prevention, diagnosis, and treatment of virus-induced liver cancer.
Maurya et al. (Tue,) studied this question.