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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Official URL: http://dx.doi.org/10.1016/j.coviro.2021.09.001 |
Abstract
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 |
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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: | https://kar.kent.ac.uk/id/eprint/90593 (The current URI for this page, for reference purposes) |
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