Mary Wilson
Well-known member
Vol. 10:- (Volume publication date September 2023)
Review in Advance first posted online on April 11, 2023. (Changes may still occur before final publication.)
https://doi.org/10.1146/annurev-virology-111821-103452
Caleb J. Studstill and Cary A. Moody
Abstract
High-risk human papillomaviruses (HPVs) are associated with several human cancers. HPVs are small, DNA viruses that rely on host cell machinery for viral replication. The HPV life cycle takes place in the stratified epithelium, which is composed of different cell states, including terminally differentiating cells that are no longer active in the cell cycle. HPVs have evolved mechanisms to persist and replicate in the stratified epithelium by hijacking and modulating cellular pathways, including the DNA damage response (DDR). HPVs activate and exploit DDR pathways to promote viral replication, which in turn increases the susceptibility of the host cell to genomic instability and carcinogenesis. Here, we review recent advances in our understanding of the regulation of the host cell DDR by high-risk HPVs during the viral life cycle and discuss the potential cellular consequences of modulating DDR pathways.
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https://www.annualreviews.org/doi/abs/10.1146/annurev-virology-111821-103452
Review in Advance first posted online on April 11, 2023. (Changes may still occur before final publication.)
https://doi.org/10.1146/annurev-virology-111821-103452
Caleb J. Studstill and Cary A. Moody
Abstract
High-risk human papillomaviruses (HPVs) are associated with several human cancers. HPVs are small, DNA viruses that rely on host cell machinery for viral replication. The HPV life cycle takes place in the stratified epithelium, which is composed of different cell states, including terminally differentiating cells that are no longer active in the cell cycle. HPVs have evolved mechanisms to persist and replicate in the stratified epithelium by hijacking and modulating cellular pathways, including the DNA damage response (DDR). HPVs activate and exploit DDR pathways to promote viral replication, which in turn increases the susceptibility of the host cell to genomic instability and carcinogenesis. Here, we review recent advances in our understanding of the regulation of the host cell DDR by high-risk HPVs during the viral life cycle and discuss the potential cellular consequences of modulating DDR pathways.
Download PDF
https://www.annualreviews.org/doi/abs/10.1146/annurev-virology-111821-103452