The human papillomavirus oncoproteins: a review of the host pathways targeted on the road to transformation

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...

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Bibliographic Details
Published inJournal of general virology Vol. 102; no. 3
Main Authors Scarth, James A., Patterson, Molly R., Morgan, Ethan L., Macdonald, Andrew
Format Journal Article
LanguageEnglish
Published England Microbiology Society 01.03.2021
Subjects
Alphapapillomavirus - genetics
Alphapapillomavirus - pathogenicity
Alphapapillomavirus - physiology
Apoptosis
Carcinogenesis
Cell Cycle Checkpoints
Cell Differentiation
Cell Proliferation
Cell Transformation, Viral
Cellular Reprogramming
Epigenesis, Genetic
Genome, Viral
Humans
Immune Evasion
Oncogene Proteins, Viral - genetics
Oncogene Proteins, Viral - metabolism
Papillomavirus Infections - virology
PDZ Domains
Review
RNA, Untranslated - genetics
Signal Transduction
Virus Replication
cancer
keratinocyte
oncoprotein
signalling
HPV
Online AccessGet full text
ISSN0022-1317
1465-2099
1465-2099
DOI10.1099/jgv.0.001540

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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.
AbstractList 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.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.
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.
Author Scarth, James A.
Morgan, Ethan L.
Macdonald, Andrew
Patterson, Molly R.
Author_xml – sequence: 1
  givenname: James A.
  orcidid: 0000-0002-0076-6853
  surname: Scarth
  fullname: Scarth, James A.
  organization: Astbury Centre for Structural Molecular Biology, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK
– sequence: 2
  givenname: Molly R.
  orcidid: 0000-0001-6246-7181
  surname: Patterson
  fullname: Patterson, Molly R.
  organization: Astbury Centre for Structural Molecular Biology, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK
– sequence: 3
  givenname: Ethan L.
  orcidid: 0000-0002-6487-5450
  surname: Morgan
  fullname: Morgan, Ethan L.
  organization: School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK, Present address: Tumour Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, National Institute of Health, Bethesda, MD 20892, USA, Astbury Centre for Structural Molecular Biology, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK
– sequence: 4
  givenname: Andrew
  orcidid: 0000-0002-5978-4693
  surname: Macdonald
  fullname: Macdonald, Andrew
  organization: School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK, Astbury Centre for Structural Molecular Biology, University of Leeds, Leeds, West Yorkshire, LS2 9JT, UK
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33427604$$D View this record in MEDLINE/PubMed
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SecondaryResourceType review_article
Snippet Persistent infection with high-risk human papillomaviruses (HR-HPVs) is the causal factor in over 99 % of cervical cancer cases, and a significant proportion...
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pubmed
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SubjectTerms Alphapapillomavirus - genetics
Alphapapillomavirus - pathogenicity
Alphapapillomavirus - physiology
Apoptosis
Carcinogenesis
Cell Cycle Checkpoints
Cell Differentiation
Cell Proliferation
Cell Transformation, Viral
Cellular Reprogramming
Epigenesis, Genetic
Genome, Viral
Humans
Immune Evasion
Oncogene Proteins, Viral - genetics
Oncogene Proteins, Viral - metabolism
Papillomavirus Infections - virology
PDZ Domains
Review
RNA, Untranslated - genetics
Signal Transduction
Virus Replication
Title The human papillomavirus oncoproteins: a review of the host pathways targeted on the road to transformation
URI https://www.ncbi.nlm.nih.gov/pubmed/33427604
https://www.proquest.com/docview/2476846843
https://pubmed.ncbi.nlm.nih.gov/PMC8148304
Volume 102
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