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A3G-induced mutations show a low prevalence and exhibit plus-strand regional distribution in hepatitis B virus DNA from patients with non-hepatocellular carcinoma (HCC) and HCC.

Authors
  • Ren, FengLing1
  • Li, WeiNa2
  • Zhao, ShuDong3
  • Wang, Li2
  • Wang, Qin2
  • Li, Meng2
  • Xiang, An2
  • Guo, YanHai2
  • 1 School of Public Health, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China. , (China)
  • 2 Department of Biopharmaceutics, Air Force Military Medical University, Xi'an, Shaanxi, China. , (China)
  • 3 YinChuan Women and Children Healthcare Hospital, Yinchuan, Ningxia, China. , (China)
Type
Published Article
Journal
Journal of Medical Virology
Publisher
Wiley (John Wiley & Sons)
Publication Date
Jun 01, 2021
Volume
93
Issue
6
Pages
3672–3678
Identifiers
DOI: 10.1002/jmv.26418
PMID: 32779759
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

APOBEC3G (A3G) cytidine deaminase is an innate immune restriction factor that can edit and inhibit hepatitis B virus (HBV) replication. The preferred target of A3G is deamination of the third cytosine of 5'CCC to form a mutant marker 5'CC C → K. However, the distribution of A3G-induced mutations on HBV DNA during infection is not well characterized. To provide clarity, we obtained the HBV DNA sequences from HBV infected individuals with and without hepatocellular carcinoma (HCC and non-HCC, respectively), from the NCBI database, and calculated the r values of A3G-induced 5'CC C → K mutation prevalence in HBV DNA. A3G-induced mutations were weakly prevalent and mainly distributed in the plus strand of HBV DNA (r = 1.407). The mutations on the minus strand were weaker (r = .8189). There were A3G-induced mutation regions in the 1200 to 2000 nt region of the plus strand and the 1600 to 1500 nt region of the minus strand. There was no significant difference in the r values of A3G-induced mutations in HBV DNA between the HCC and non-HCC groups. However, the rvalue of the plus strand 2400 to 2800 nt regions of HCC derived HBV DNA (r = 4.2) was significantly higher than that of the same regions of non-HCC derived HBV DNA (r = 1.21). These findings clarify the weak prevalence and preferred plus-strand distribution of A3G-induced mutations on HBV DNA from HCC and non-HCC. These findings may provide valuable clues regarding the interaction mechanism between A3G and HBV DNA and inform HCC screening. © 2020 Wiley Periodicals LLC.

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