AI Article Synopsis
- Viral hepatitis B (HBV) and hepatitis C (HCV) are major risk factors for hepatocellular carcinoma (HCC), with their varying prevalence affecting global liver cancer rates.
- Chronic infection from these viruses leads to ongoing liver inflammation and may result in severe conditions like liver fibrosis and cirrhosis, ultimately increasing the risk for HCC development.
- The review aims to discuss epidemiological aspects of HBV and HCV, delve into the immune responses to these infections, and analyze how the resulting immune environment contributes to the advancement of HCC.
Article Abstract
Viral hepatitis B (HBV) and hepatitis C (HCV) infections remain the most common risk factors for the development of hepatocellular carcinoma (HCC), and their heterogeneous distribution influences the global prevalence of this common type of liver cancer. Typical hepatitis infection elicits various immune responses within the liver microenvironment, and viral persistence induces chronic liver inflammation and carcinogenesis. HBV is directly mutagenic but can also cause low-grade liver inflammation characterized by episodes of intermittent high-grade liver inflammation, liver fibrosis, and cirrhosis, which can progress to decompensated liver disease and HCC. Equally, the absence of key innate and adaptive immune responses in chronic HCV infection dampens viral eradication and induces an exhausted and immunosuppressive liver niche that favors HCC development and progression. The objectives of this review are to (i) discuss the epidemiological pattern of HBV and HCV infections, (ii) understand the host immune response to acute and chronic viral hepatitis, and (iii) explore the link between this diseased immune environment and the development and progression of HCC in preclinical models and HCC patients.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8909759 | PMC |
| http://dx.doi.org/10.3390/cancers14051255 | DOI Listing |
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