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Indian J Med Microbiol ; 2019 Sep; 37(3): 387-392
Artigo | IMSEAR | ID: sea-198890

RESUMO

Introduction: Hepatitis B virus (HBV) is the most common aetiological factor causing hepatocellular carcinoma (HCC). HBx gene plays an enigmatic role in HBV-related HCC. In this study we have analysed amino acid substitutions in HBx from HBV-infected individuals of different clinical stages. Materials and Methods: HBV-infected individuals (n = 93) were recruited in the study. DNA was extracted from plasma, amplified, and DNA sequencing was performed using specific primers targeting HBx gene (540 bp). Results: Among the study participants, 57% had chronic HBV infection, 30% had chronic liver disease (CLD) and 13% had HBV related HCC. Genotypes such as D1, D2, D3, A1, C2 and B2 were identified of which genotype D2 was predominant (78%). HBxC-terminal deletion was observed in four hepatitis B e antigen (HBeAg) negative participants with CLD. The frequency of aminoacid substitution in proapoptotic domain was higher in HBeAg negative participants including I127V (34%), K130M (34%), V131I (40%). The frequency of double mutation (K130M+V131I) and triple mutation (I127V+K130M+V131I) were found to be higher (32% and 36%) in HBeAg negative participants. Also, we identified L5M substitution (4.3%) in HBeAg positive participants with advanced liver disease. Conclusion: In HBx gene, aminoacid substitutions at positions 127, 130, 131 are associated with poor expression of HBeAg. We suggest screening for HBx aminoacid substitutions especially in patients with HBeAg negative chronic HBV infection to predict the clinical outcome and enable early treatment to prevent disease progression.

2.
Artigo em Chinês | WPRIM | ID: wpr-679583

RESUMO

ChildA (4.54%,x~2= 21.992,P=0.000);Among the HBeAg positive patients,the mortality of MELD≥ 18 patients (17.24%) was higher than the MELDChild A (0%,x~2= 5.363,P=0.021).Multivariate analysis showed that death rate was independently predicted by old age,higher Child -Pugh and the ALT persistent elevation in hepatitis B e antigen-negative patients with liver cirrhosis (P

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