All authors declare that they have no conflict of interest.
Article first published online: 28 SEP 2012
Copyright © 2012 Wiley Periodicals, Inc.
Journal of Medical Virology
Volume 85, Issue 1, pages 16–25, January 2013
How to Cite
Tangkijvanich, P., Sa-Nguanmoo, P., Avihingsanon, A., Ruxrungtham, K., Poovorawan, K. and Poovorawan, Y. (2013), Characterization of hepatitis B virus mutations in untreated patients co-infected with HIV and HBV based on complete genome sequencing. J. Med. Virol., 85: 16–25. doi: 10.1002/jmv.23430
Ethical approval: The study was approved by the Ethics Committee, Faculty of Medicine, Chulalongkorn University.
- Issue published online: 13 NOV 2012
- Article first published online: 28 SEP 2012
- Manuscript Accepted: 20 AUG 2012
- Liver Research Unit and the Center of Excellence in Clinical Virology, Chulalongkorn University
- Higher Education Research Promotion and National Research University Project of Thailand. Grant Numbers: HR1162A-55, HR1155A-55
- Office of the Higher Education Commission, the Commission on Higher Education
- Thailand Research Fund. Grant Numbers: BRG5580005, DPG5480002, TRG5480012
- Postdoctoral Fellowship (Ratchadaphiseksomphot Endowment Fund)
- CU Centenary Academic Development Project
- King Chulalongkorn Memorial Hospital
- hepatitis B virus;
- genome sequencing;
Co-infection of HBV with HIV results in an accelerated course of HBV-associated chronic liver disease. Several studies have shown that viral mutations are related to disease progression in mono-infection with HBV. However, it is unclear whether HBV mutation patterns might differ between co-infected and mono-infected patients. To compare the frequencies and mutation patterns in the HBV genome between co-infection and mono-infection. Twenty-four treatment-naïve co-infected and 31 treatment-naïve mono-infected Thai patients were included. HBV mutations were characterized by whole genome sequencing of virus serum samples. The clinical features and frequency of known clinically significant mutations were compared between the two groups. No significant difference between the groups was found with respect to sex, age and HBeAg. However, HBV DNA levels were significantly higher in co-infected patients. The distribution of HBV genotypes was comparable between the two groups and restricted mostly to sub-genotypes C1 and B2. An isolate with recombinants of genotypes G/C1 was also identified in a patient with co-infection. There was no difference in the prevalence of mutations in the enhancer II/basal core promoter/precore region, pre-S/S and polymerase genes between the two groups. In conclusion, dual infections tend to engender increased HBV DNA levels. There was no major difference in the frequencies of common HBV mutations between co-infected and mono-infected patients. Thus, HBV mutations may not contribute to disease pathogenesis in Thai patients with co-infection. J. Med. Virol. 85:16–25, 2012. © 2012 Wiley Periodicals, Inc.