Gene X Two Triple Mutations Predominance on Chronic Hepatitis B Virus in Padang, West Sumatra Indonesia

Afida Razuna Ave(1), Andani Eka Putra(2), Saptino Miro(3),

(1) Master Program in Biomedical Sciences, Faculty of Medicine, Universitas Andalas, Padang
(2) Department of Microbiology, Faculty of Medicine, Universitas Andalas, Padang
(3) Department of Internal Medicine, Faculty of Medicine, Universitas Andalas/M. Djamil General Hospital, Padang
Corresponding Author


Background: Hepatitis B is a health issue that become major problem worldwide with high morbidity. Hepatitis B is a liver infection that caused by Hepatitis B Virus. Chronic hepatitis B is a liver inflammation that lasted more than 6 months and it has the potential to progress to liver cirrhosis and hepatocellular cancer. The disease is influenced by Gene X and viral genotype. Mutations in the Gene X are suspected to having a role in disease progression. The aim of this study was to detect Gene X polymorphism and the phylogeny of HBV from Padang local clinical samples of chronic hepatitis B (CHB), West Sumatera, Indonesia.

Method: The entire chronically HBV-infected patients were enrolled in this study: 38 CHB. The research samples were the entire Hepatitis B serum from Indonesian Red Cross Blood Bank than Gene X was amplified using nested PCR, which produced two fragments and aligned with X sequence database continued with mutation analysis.

 Results: In this study we found all the samples were having nucleotide variation. Of various mutations, we observed the presence of known liver cirrhosis and HCC-related HBx protein mutant i.e double mutations (HBx130 and HBx131) and two triple mutations (HBx5/HBx130/HBx131) and (HBx127/HBx130/HBx131) were high. The analysis also showed that patients were infected mainly by genotype C at 72,2% and followed by B at 27,8%.

Conclusion: We conclude that all the samples have nucleotide variation and the mutation implying that molecular progression between the virus and the host at chronically infected patients.


Hepatitis B virus; gene X; mutation

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DOI: 10.24871/2322022206-211


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