ArticleInfectious agents and cancer2026
Novel C-terminal HBx truncation (G135) in genotype D1 HBV: predicted effects on oncogenic signaling.
Article in Infectious agents and cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Combined C-terminal truncation and point mutations in HBx in genotype D1 HBV-associated hepatocellular carcinoma.Infectious agents and cancer · 2026Article
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4 authors.
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Abstract
BACKGROUND &
aimsHepatitis B virus X protein (HBx) is a multifunctional viral regulator implicated in hepatocellular carcinoma (HCC). We aimed to characterize HBx mutations in liver tissue samples from Iranian patients with HCC and explore their potential structural and functional implications.
methodsLiver tissue samples from 10 patients with HCC and chronic HBV infection were analyzed using high-resolution melting (HRM) and Sanger sequencing. Detected variants were assessed by phylogenetic analysis, 3D protein modeling, and STRING-based protein–protein interaction (PPI) mapping. Correlations with clinical and biochemical parameters were examined.
resultsMultiple HBx mutations were identified, including a novel nonsense mutation at codon 135 (G135*), resulting in C-terminal truncation. Additional substitutions were found in the H-box (V88A, K94E, A100T), BH3-like motif (L113P, Q116R, E122K, A126T), and CCCH zinc-binding domain (C61S, C69R). Structural modeling predicted that these variants may potentially disrupt DDB1 and Bcl-2 interactions, as well as zinc coordination. STRING analysis suggested altered HBx connectivity with TP53, BAX, TNF, IL6, and CREB1, potentially affecting apoptosis, transcriptional regulation, and inflammatory signaling. Phylogenetic analysis confirmed that variants clustered within genotype D1, indicating intra-genotypic adaptation. Clinically, higher viral loads and HBeAg positivity were associated with elevated liver injury markers, consistent with the predicted functional impacts of these variants.
conclusionsHBx mutations in genotype D1, particularly the novel C-terminal truncation, may potentially influence viral persistence, apoptotic resistance, and oncogenic signaling in HCC, pending experimental validation. These findings highlight intra-genotypic HBx diversity as a potential biomarker and therapeutic target for HBV-related liver cancer. CLINICAL TRIAL NUMBER: Not applicable.
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