Innate and Adaptive Immunopathogeneses in Viral Hepatitis; Crucial Determinants of Hepatocellular Carcinoma.
Marco Y W ZakiAhmed M FathiSamara SamirNardeen EldafashiKerolis Y WilliamMaiiada Hassan NazmyMoustafa FathyUpkar S GillShishir ShettyPublished in: Cancers (2022)
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.
Keyphrases
- immune response
- low grade
- liver failure
- high grade
- sars cov
- hepatitis b virus
- hepatitis c virus
- oxidative stress
- liver fibrosis
- heart failure
- end stage renal disease
- ejection fraction
- drug induced
- stem cells
- newly diagnosed
- toll like receptor
- prognostic factors
- peritoneal dialysis
- intensive care unit
- mesenchymal stem cells
- helicobacter pylori
- inflammatory response
- respiratory failure
- aortic dissection