Persistent Human Papillomavirus Infection.
HPV
cancer
epithelium
extrachromosomal replication
immune evasion
latency
papillomavirus
persistence
tethering
Journal
Viruses
ISSN: 1999-4915
Titre abrégé: Viruses
Pays: Switzerland
ID NLM: 101509722
Informations de publication
Date de publication:
20 02 2021
20 02 2021
Historique:
received:
16
01
2021
revised:
16
02
2021
accepted:
17
02
2021
entrez:
6
3
2021
pubmed:
7
3
2021
medline:
13
8
2021
Statut:
epublish
Résumé
Persistent infection with oncogenic human papillomavirus (HPV) types is responsible for ~5% of human cancers. The HPV infectious cycle can sustain long-term infection in stratified epithelia because viral DNA is maintained as low copy number extrachromosomal plasmids in the dividing basal cells of a lesion, while progeny viral genomes are amplified to large numbers in differentiated superficial cells. The viral E1 and E2 proteins initiate viral DNA replication and maintain and partition viral genomes, in concert with the cellular replication machinery. Additionally, the E5, E6, and E7 proteins are required to evade host immune responses and to produce a cellular environment that supports viral DNA replication. An unfortunate consequence of the manipulation of cellular proliferation and differentiation is that cells become at high risk for carcinogenesis.
Identifiants
pubmed: 33672465
pii: v13020321
doi: 10.3390/v13020321
pmc: PMC7923415
pii:
doi:
Substances chimiques
DNA, Viral
0
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Intramural NIH HHS
ID : ZIA AI000713
Pays : United States
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