期刊
VIRUSES-BASEL
卷 9, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/v9080233
关键词
papillomavirus; human papillomavirus (HPV); apolipoprotein B messenger RNA-editing; enzyme-catalytic; polypeptide-like 3 (APOBEC3); innate immunity; virus restriction; cancer mutagenesis; cancer progression; somatic mutation; virus evolution
类别
资金
- National Institutes of Health [R01 AI091968, R01 DE026125, T32 AI052066]
- Technology Research Initiative Fund of Arizona
- US Department of Agriculture-National Institute of Food and Agriculture [Hatch 1012632]
The apolipoprotein B messenger RNA-editing, enzyme-catalytic, polypeptide-like 3 (APOBEC3) family of cytidine deaminases plays an important role in the innate immune response to viral infections by editing viral genomes. However, the cytidine deaminase activity of APOBEC3 enzymes also induces somatic mutations in host genomes, which may drive cancer progression. Recent studies of human papillomavirus (HPV) infection and disease outcome highlight this duality. HPV infection is potently inhibited by one family member, APOBEC3A. Expression of APOBEC3A and APOBEC3B is highly elevated by the HPV oncoproteins E6 and E7 during persistent virus infection and disease progression. Furthermore, there is a high prevalence of APOBEC3A and APOBEC3B mutation signatures in HPV-associated cancers. These findings suggest that induction of an APOBEC3-mediated antiviral response during HPV infection may inadvertently contribute to cancer mutagenesis and virus evolution. Here, we discuss current understanding of APOBEC3A and APOBEC3B biology in HPV restriction, evolution, and associated cancer mutagenesis.
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