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Abstract
Persistent infection with high-risk human papillomaviruses (HR-HPVs) is the causal factor in over 99 % of cervical cancer cases, and a significant proportion of oropharyngeal and anogenital cancers. The key drivers of HPV-mediated transformation are the oncoproteins E5, E6 and E7. Together, they act to prolong cell-cycle progression, delay differentiation and inhibit apoptosis in the host keratinocyte cell in order to generate an environment permissive for viral replication. The oncoproteins also have key roles in mediating evasion of the host immune response, enabling infection to persist. Moreover, prolonged infection within the cellular environment established by the HR-HPV oncoproteins can lead to the acquisition of host genetic mutations, eventually culminating in transformation to malignancy. In this review, we outline the many ways in which the HR-HPV oncoproteins manipulate the host cellular environment, focusing on how these activities can contribute to carcinogenesis.
Highlights
Papillomaviruses are small non-enveloped icosahedral viruses, possessing a circular double-stranded DNAgenome of approximately 8 kb in length [1]
This link between human papillomaviruses (HPVs) infection and cancer was first established over 35 years ago when HPV16 DNA was found to be present in a large proportion of cervical cancer biopsies [5]
These, together with the other oncoprotein functions discussed in this review, act to stimulate proliferation, delay differentiation, inhibit apoptosis and evade immune detection
Summary
Papillomaviruses are small non-enveloped icosahedral viruses, possessing a circular double-stranded DNA (dsDNA)genome of approximately 8 kb in length [1]. The study of human papillomaviruses (HPVs) has largely been driven by the severity of HPV-a ssociated pathologies: whilst the HPVs that infect the cutaneous epithelium and typically result in benign wart or verruca formation, as well as the low-risk mucosal HPV types 6 and 11 associated with genital warts, have received some attention, the greatest focus has been on the high-risk HPVs (HR-HPVs) associated with the development of cancer [1, 4] This link between HPV infection and cancer was first established over 35 years ago when HPV16 DNA was found to be present in a large proportion of cervical cancer biopsies [5]. HR-H PV infection is associated with cancers at a variety of other anogenital sites: around 50% of penile, 25 % of vulvar, 80 % of vaginal and close to 90 % of anal cancers are HPV-driven [10]
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