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Fig. 1 | BMC Medicine

Fig. 1

From: Occult infection with hepatitis B virus PreS variants synergistically promotes hepatocellular carcinoma development in a high-fat diet context by generating abnormal ceramides

Fig. 1

Replication-component HBV with extensive PreS/S mutations in in HBsAg-seronegative HCC patients. A Scatter diagrams show HBV rcDNA detected in 5 representative sera from the 35 HBsAg-seronegative HCC patients; the electrophoresis image shows the 332-bp products of the HBV gap region amplified from genomic DNA of liver tissues. Histological images show the representative HBsAg immunohistochemistry staining of tissue sections from the 35 HCC patients. B Mutations across PreS/S regions in 35 HBsAg-seronegative HCC patients. The isolate GU434374 from one HBsAg-seropositive HCC patient was used as the reference (Ref-HBV). Digits indicate the amino acid (AA) sites where mutations occurred. AA properties of Ref-HBV are shown below the digits, the mutated are above digits. Arrows indicate mutations occurred with no alteration in AA properties. “” indicates deletion, “*” indicates stop codon. C PreS/S AA sequences in 7 HBsAg-seronegative HCC patients were identical to Ref-HBV. Six types of PreS/S mutations were recognized in the other 28 patients. mt-I (22 cases), PreS/S AA properties differ from Ref-HBV; mt-II (1 case), PreS2 deletion at 16–22 and different AA properties from Ref-HBV; mt-III (1 case), a mutated PreS2 start codon; mt-IV (1 case), a mutated S start codon; mt-V (1 case), a new stop codon introduced at position 9 of PreS2; mt-VI (2 cases), deletions at position 69 and 112 of S gene

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