Abstract
High-risk human papillomaviruses (HPVs) are the causative agents of cervical and other genital cancers. In addition, HPV infections are associated with the development of many oropharyngeal cancers. HPVs activate and repress a number of host cellular pathways to promote their viral life cycles, including those of the DNA damage response. High-risk HPVs activate the ataxia telangiectasia-mutated (ATM) and ATM and Rad3-related (ATR) DNA damage repair pathways, which are essential for viral replication (particularly differentiation-dependent genome amplification). These DNA repair pathways are critical in maintaining host genomic integrity and stability and are often dysregulated or mutated in human cancers. Understanding how these pathways contribute to HPV replication and transformation may lead to the identification of new therapeutic targets for the treatment of existing HPV infections.
Highlights
Human papillomaviruses (HPVs) are small, non-enveloped viruses that infect cutaneous and mucosal epithelial cells of the hands, feet, oropharyngeal, and anogenital tracts
MRNA and protein levels, which hindered the downstream phosphorylation and activation of p53 in response to ultraviolet B (UVB)-induced damage [76]. These findings suggest that coordinating the activation and repression of DNA damage response pathway components is a shared, and necessary, step between HPV types for completion of the viral life cycle
Human papillomaviruses have adapted several mechanisms to ensure the completion of their viral life cycles, including the use of host cellular machinery to replicate their genomes
Summary
Human papillomaviruses (HPVs) are small, non-enveloped viruses that infect cutaneous and mucosal epithelial cells of the hands, feet, oropharyngeal, and anogenital tracts. Alpha-genus HPVs that infect the genital tract are further classified as either low- or high-risk based on their association with the development of cancers [1,2]. Ten HPV types, including HPV16, 18, 31, and 45, are considered the etiological agents of cervical cancer, as they are detected in over 99% of cervical carcinomas [3]. These high-risk HPVs have been linked to the development of anal, vulvar, vaginal, and penile cancers, as well as a rising number of cancers of the oropharyngeal region [4,5]. As there currently is no treatment for HPV infection outside of surgery or cryotherapy, understanding the involvement of these pathways in regulating the viral life cycle may lead to new treatment options and further decrease the incidence of HPV-associated carcinomas [10]
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