ArticleHepatology communications2026
Distinct immune signatures define hepatitis D- versus hepatitis B-associated hepatocellular carcinoma.
Article in Hepatology communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. Hepatitis D is the most severe form of viral hepatitis. However, the clinical, virological, and systemic inflammatory characteristics of HDV-associated HCC remain insufficiently characterized.
methodsIn this single-center retrospective study, we identified 162 patients with HCC due to chronic hepatitis D (HDV-HCC; n=54) or chronic hepatitis B (HBV-HCC; n=108). Plasma levels of 92 soluble inflammatory mediators (SIMs) were quantified using proximity extension assay in HCC patients [HBV-HCC (n=50), HDV-HCC (n=30), and matched non-HCC controls (HBV=19, HDV=17)].
resultsAt the time of HCC diagnosis, patients with CHD were younger, had more impaired liver synthesis and detoxification function, and lower levels of AST, CRP, and leukocytes. HDV-HCCs presented with smaller tumors, less frequent portal vein infiltration, and more often fulfilled Milan criteria (all p<0.01). Systemic immune profiling revealed distinct inflammatory patterns between both etiologies. Compared with HBV-HCC, HDV-HCC was characterized by a comparatively stronger IL-10-associated immunoregulatory signature, whereas HBV-HCC exhibited a more pronounced pro-inflammatory profile involving IL-6- and phosphorylation- and proliferation-associated signaling. Despite these differences, event-free survival did not differ between groups.
conclusionsHBV-HCC more frequently presented with advanced tumor stage, whereas HDV-HCC was associated with more severe underlying liver disease but smaller tumors. Importantly, HBV-associated and HDV-associated HCC exhibit distinct systemic inflammatory signatures, potentially reflecting differences in systemic immune regulation between etiologies. These findings may have implications for biomarker development and future etiology-specific therapeutic strategies.
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