Research Paper Volume 8, Issue 11 pp 2862—2870
Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naïve patients
- 1 Xiamen Center for Disease Control and Prevention, Xiamen, Fujian 361021, China
- 2 School of Public Health, Fujian Medical University, Fuzhou, Fujian 351022, China
- 3 Xiamen Hospital of Traditional Chinses Medicine, Xiamen, Fujian 361001, China
- 4 Roche Pharma Research and Early Development, Immunology, Inflammation and Infectious Diseases, Roche Innovation Center Shanghai 201203, China
- 5 Roche Pharma Research and Early Development, Immunology, Inflammation and Infectious Diseases, Roche Innovation Center Basel 4070, Switzerland
- 6 Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, China
Received: August 12, 2016 Accepted: October 24, 2016 Published: November 7, 2016
https://doi.org/10.18632/aging.101097How to Cite
Abstract
Mannose binding lectin (MBL) plays important role in the innate immunity of human. Mutations in the MBL2 gene can significantly change the serum level of MBL, and consequently alter the susceptibility and progression of infectious disease. However, the association between the MBL2 profile and the HBV mutation and quasispecies complexity has not yet been reported. Our approach includes the study of the MBL2 gene genotype as well as ultra-deep sequencing of the HBV viruses obtained from the plasma of 50 treatment naïve patients with chronic HBV infection. We found that the liver function was better among patients within the high MBL2 group with respect to those within the medium/low MBL2 group. Likewise, the number of mutations in the HBV X gene as well as the viral quasispecies complexity were significantly higher in medium/low MBL2 production group. Nucleotide substitution rates were also higher within the medium/low MBL2 production group in all positions described to have an influence in liver cancer development, except for A1499G. In this work we show that the MBL2 profile may have an impact on the HBV X gene mutations as well as on viral quasispecies complexity.