Published online Jun 7, 2022. doi: 10.3748/wjg.v28.i21.2251
Peer-review started: September 13, 2021
First decision: November 16, 2021
Revised: December 8, 2021
Accepted: April 26, 2022
Article in press: April 26, 2022
Published online: June 7, 2022
Processing time: 261 Days and 13.8 Hours
Hepatocellular carcinoma (HCC) is a global health challenge. Due to the high prevalence in low-income countries, hepatitis B virus (HBV) and hepatitis C virus infections remain the main risk factors for HCC occurrence, despite the increasing frequencies of non-viral etiologies. In addition, hepatitis D virus coinfection increases the oncogenic risk in patients with HBV infection. The molecular processes underlying HCC development are complex and various, either independent from liver disease etiology or etiology-related. The reciprocal interlinkage among non-viral and viral risk factors, the damaged cellular microenvironment, the dysregulation of the immune system and the alteration of gut-liver-axis are known to participate in liver cancer induction and progression. Oncogenic mechanisms and pathways change throughout the natural history of viral hepatitis with the worsening of liver fibrosis. The high risk of cancer incidence in chronic viral hepatitis infected patients compared to other liver disease etiologies makes it necessary to implement a proper surveillance, both through clinical-biochemical scores and periodic ultrasound assessment. This review aims to outline viral and microenvironmental factors contributing to HCC occurrence in patients with chronic viral hepatitis and to point out the importance of surveillance programs recommended by international guidelines to promote early diagnosis of HCC.
Core Tip: Chronic hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV) infection represents a global health burden leading to liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Among these complications, HCC accounts for 3.5% of all deaths worldwide. Thus, the understanding of the role of chronic hepatitis virus infection in HCC development is necessary in order to clarify the mechanisms underlying oncogenesis and design future treatments for this cancer. This review outlines pathophysiological and molecular pathways that contribute to carcinogenesis in HBV, HCV and HDV chronic infection focusing on the impact of clinical surveillance and antiviral treatment on the risk of HCC development.