Persistent Human Papillomavirus Infection. Della Fera, A. N., Warburton, A., Coursey, T. L., Khurana, S., & McBride, A. A. 13(2):321.
doi  abstract   bibtex   
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.
@article{della_fera_persistent_2021,
	title = {Persistent Human Papillomavirus Infection},
	volume = {13},
	issn = {1999-4915},
	doi = {10.3390/v13020321},
	abstract = {Persistent infection with oncogenic human papillomavirus ({HPV}) types is responsible for {\textasciitilde}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.},
	pages = {321},
	number = {2},
	journaltitle = {Viruses},
	shortjournal = {Viruses},
	author = {Della Fera, Ashley N. and Warburton, Alix and Coursey, Tami L. and Khurana, Simran and {McBride}, Alison A.},
	date = {2021-02-20},
	pmid = {33672465},
	pmcid = {PMC7923415},
	keywords = {cancer, papillomavirus, {HPV}, Humans, Papillomavirus Infections, Virus Replication, latency, Papillomaviridae, persistence, {DNA}, Viral, Animals, epithelium, extrachromosomal replication, Genome, Viral, immune evasion, tethering},
	file = {Plný text:C\:\\Users\\Miroslava Kuderavá\\Zotero\\storage\\PG4QMPJY\\Della Fera et al. - 2021 - Persistent Human Papillomavirus Infection.pdf:application/pdf},
}

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