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Hepatitis B virus (HBV) is a known cause of hepatocellular carcinoma (HCC). The role of HBx gene in HBV-related HCC is not yet clearly understood. Therefore, in a recent study conducted in Tamil Nadu, India, investigators studied amino acid substitutions in HBx from HBV-infected individuals of different clinical stages.
Ninety three HBV-infected subjects were enrolled in the study. Investigators extracted the DNA from plasma, and performed DNA sequencing using specific primers targeting HBx gene (540 bp).
Overall, 57% of the study subjects had chronic HBV infection, 30% had chronic liver disease (CLD) and 13% had HBV-related HCC. Of the identified genotypes, including D1, D2, D3, A1, C2 and B2, genotype D2 was predominant (78%). There was evidence of HBxC-terminal deletion in four hepatitis B e antigen (HBeAg)-negative participants with CLD. The frequency of amino acid substitution in proapoptotic domain was higher in HBeAg-negative subjects, including I127V (34%), K130M (34%), V131I (40%). Additionally, double mutation (K130M+V131I) and triple mutation (I127V+K130M+V131I) were also more frequent (32% and 36%) in HBeAg-negative participants. L5M substitution (4.3%) was noted in HBeAg-positive patients with advanced liver disease.
To conclude, in HBx gene, amino acid substitutions at positions 127, 130, 131 appeared to be linked with poor expression of HBeAg. Screening for HBx amino acid substitutions is thus advised, particularly in patients with HBeAg-negative chronic HBV infection in a bid to facilitate early treatment initiation to prevent disease progression.
Source: Mani M, Vijayaraghavan S, Sarangan G, et al. Hepatitis B virus X protein: The X factor in chronic hepatitis B virus disease progression. Indian J Med Microbiol. 2019 Jul-Sep;37(3):387-392.