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Persistent Human Papillomavirus Infection
by
Coursey, Tami L.
, Della Fera, Ashley N.
, Warburton, Alix
, Khurana, Simran
, McBride, Alison A.
in
cancer
/ carcinogenesis
/ cell proliferation
/ chronic diseases
/ DNA replication
/ extrachromosomal replication
/ HPV
/ humans
/ Papillomaviridae
/ papillomavirus
/ persistence
/ plasmids
/ progeny
/ Review
/ risk
/ tethering
/ viral genome
2021
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Persistent Human Papillomavirus Infection
by
Coursey, Tami L.
, Della Fera, Ashley N.
, Warburton, Alix
, Khurana, Simran
, McBride, Alison A.
in
cancer
/ carcinogenesis
/ cell proliferation
/ chronic diseases
/ DNA replication
/ extrachromosomal replication
/ HPV
/ humans
/ Papillomaviridae
/ papillomavirus
/ persistence
/ plasmids
/ progeny
/ Review
/ risk
/ tethering
/ viral genome
2021
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While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Persistent Human Papillomavirus Infection
by
Coursey, Tami L.
, Della Fera, Ashley N.
, Warburton, Alix
, Khurana, Simran
, McBride, Alison A.
in
cancer
/ carcinogenesis
/ cell proliferation
/ chronic diseases
/ DNA replication
/ extrachromosomal replication
/ HPV
/ humans
/ Papillomaviridae
/ papillomavirus
/ persistence
/ plasmids
/ progeny
/ Review
/ risk
/ tethering
/ viral genome
2021
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Journal Article
Persistent Human Papillomavirus Infection
2021
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Overview
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.
Publisher
MDPI,MDPI AG
Subject
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