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Accumulation of Host Cell Genetic Errors following High-Risk HPV Infection

Fenton, Tim R (2021) Accumulation of Host Cell Genetic Errors following High-Risk HPV Infection. Current Opinion in Virology, 51 . pp. 1-8. ISSN 1879-6257. (doi:10.1016/j.coviro.2021.09.001) (KAR id:90593)

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APOBEC3 cytidine deaminases convert deoxycytidine to deoxyuridine in single-stranded DNA, forming part of the innate immune response to HPV infection but also contributing to mutagenesis of the host genome of infected cells during HPV-associated carcinogenesis. Of the seven human APOBEC3 genes, two (APOBEC3A and APOBEC3B) have been implicated in both processes, with evidence increasingly pointing to APOBEC3A as the main culprit in somatic mutagenesis. This review discusses recent developments in host and viral genome sequencing that suggests viral editing by one or more APOBEC3 enzymes plays an important role in viral clearance, while bursts of APOBEC3A activity may drive carcinogenesis in persistently infected cells. Progress in our understanding of HPV replication is also discussed and a model is presented in which chronic activation of the DNA damage response by HPV, together with suppression of p53 function acts to create a perfect storm for APOBEC3 activity against the host cell genome.

Item Type: Article
DOI/Identification number: 10.1016/j.coviro.2021.09.001
Uncontrolled keywords: APOBEC HPV cancer
Subjects: Q Science > QP Physiology (Living systems) > QP506 Molecular biology
Q Science > QR Microbiology > QR180 Immunology
Q Science > QR Microbiology > QR355 Virology
Divisions: Divisions > Division of Natural Sciences > Biosciences
Depositing User: Tim Fenton
Date Deposited: 05 Oct 2021 10:09 UTC
Last Modified: 17 Sep 2022 23:00 UTC
Resource URI: (The current URI for this page, for reference purposes)
Fenton, Tim R:
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