From:  HLA-KIRs interactions in modulating natural killer cell responses against viral hepatitis: a concise review

 Comparative analysis of HLA expression in HBV and HCV infections.

FeaturesHBVHCVReferences
HLA-I expressionUpregulation of hepatocytes enhances CD8+ T cell recognition but promotes immune-mediated liver injuryConsistent upregulation in hepatocytes supports sustained immune surveillance[41]
Viral protein interferenceHBV X protein downregulates HLA-I, enabling viral escape and persistenceHCV core, NS3, and NS5A proteins interfere with antigen processing, reducing peptide loading[38]
Regulation patternBidirectional: upregulation vs. suppression depending on stage and immune contextPredominantly upregulation with indirect suppression via antigen-processing disruption[42]
HLA-II expressionAberrant induction of hepatocytes and cholangiocytes, associated with chronic inflammation and autoimmune-like pathologySimilar aberrant induction fuels intrahepatic inflammation and autoimmune-like injury[43]
Immune evasion strategyDirect suppression of surface HLA expression by viral proteinsDisruption of antigen processing machinery, broader upstream dysregulation[44]
Clinical implicationsBalance between viral clearance and immune-mediated injury; linked to fibrosis progressionPersistent immune activation but dampened cytotoxicity; linked to chronicity and HCC risk[45]

HBV: hepatitis B virus; HCC: hepatocellular carcinoma; HCV: hepatitis C virus; HLA: human leukocyte antigen.