Abstract
The DNA damage response (DDR) maintains genomic integrity through an elaborate network of signaling pathways that sense DNA damage and recruit effector factors to repair damaged DNA. DDR signaling pathways are usurped and manipulated by the replication programs of many viruses. Here, we review the papillomavirus (PV) life cycle, highlighting current knowledge of how PVs recruit and engage the DDR to facilitate productive infection.
Highlights
Papillomaviruses (PVs) are an ancient group of small, double-stranded DNA viruses that infect the highly adapted niche of the stratified epithelium of the skin or mucosa in specific host species. HPV infection can be asymptomatic, HPVs are the etiological agent of a wide range of benign papillomas or warts [1]
Initial evidence using bovine papillomavirus type 1 (BPV1) suggested that viral genome replication is licensed during the maintenance phase [27,28], but later studies demonstrated that in S-phase cells, replication is by a random choice mechanism, whereby some genomes undergo multiple rounds of replication and others remain unreplicated [29,30]
The damage response and repair (DDR) consists of sensors, such as the MRE11-Rad50-Nbs1 complex (MRN) or replication protein A (RPA), that detect a wide range of DNA lesions and recruit the Ataxia telangiectasia mutated (ATM) and Ataxia telangiectasia and Rad3 related (ATR) transducer kinases to the site of damage
Summary
Papillomaviruses (PVs) are an ancient group of small, double-stranded (ds) DNA viruses that infect the highly adapted niche of the stratified epithelium of the skin or mucosa in specific host species. E), late promoter (PL) and early and late polyadenylation sites (pAE and pAL) are indicated Because of this limited coding capacity, PVs retain a strict dependence on host factors for viral. Of this limited of coding capacity, PVs retain a strict dependence on host factors viral replication. Elucidation the different replication mechanisms of HPV could identify novelfortargets replication [6]. HPV infections, where the multivalent vaccines are not readily useful. We review the mechanisms of replication in the HPV life cycle summarize how the virus recruits and engages the DDR of genome replication in the life cycle and summarize how the virus recruits and engages the DDR to facilitate viral DNA synthesis
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