APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?

被引：25

作者：

Warren, Cody J. ^{[1
]}

Santiago, Mario L. ^{[2
]}

Pyeon, Dohun ^{[3
]}

机构：

[1] Univ Colorado, BioFrontiers Inst, Boulder, CO 80309 USA

[2] Univ Colorado, Dept Med, Div Infect Dis, Anschutz Med Campus, Aurora, CO 80045 USA

[3] Michigan State Univ, Dept Microbiol & Mol Genet, E Lansing, MI 48824 USA

来源：

ANNUAL REVIEW OF VIROLOGY | 2022年 / 9卷

基金：

美国国家卫生研究院;

关键词：

DNA CYTOSINE DEAMINASE; CYTIDINE DEAMINASES; BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; MUTATIONAL SIGNATURES; DELETION POLYMORPHISM; SOMATIC MUTATIONS; UP-REGULATION; MUTAGENESIS; EXPRESSION;

D O I：

10.1146/annurev-virology-092920-030354

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Human papillomavirus (HPV) infection is a causative agent of multiple human cancers, including cervical and head and neck cancers. In these HPV-positive tumors, somatic mutations are caused by aberrant activation of DNA mutators such as members of the apolipoprotein B messenger RNA-editing enzyme catalytic polypeptide-like 3 (APOBEC3) family of cytidine deaminases. APOBEC3 proteins are most notable for their restriction of various viruses, including anti-HPV activity. However, the potential role of APOBEC3 proteins in HPV-induced cancer progression has recently garnered significant attention. Ongoing research stems from the observations that elevated APOBEC3 expression is driven by HPV oncogene expression and that APOBEC3 activity is likely a significant contributor to somatic mutagenesis in HPV-positive cancers. This review focuses on recent advances in the study of APOBEC3 proteins and their roles in HPV infection and HPV-driven oncogenesis. Further, we discuss critical gaps and unanswered questions in our understanding of APOBEC3 in virus-associated cancers.

引用

页码：375 / 395

页数：21

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