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J Virol. 2012 Jun;86(11):6358-64. doi: 10.1128/JVI.07069-11. Epub 2012 Mar 28.

Reconstruction of human papillomavirus type 16-mediated early-stage neoplasia implicates E6/E7 deregulation and the loss of contact inhibition in neoplastic progression.

Author information

1
Division of Virology, National Institute for Medical Research, London, United Kingdom.

Abstract

Infection with human papillomavirus type 16 (HPV-16) can lead to low- or high-grade squamous intraepithelial lesions (LSIL or HSIL). Here we show that these in vivo disease states can be replicated in raft cultures of early-pass HPV-16 episomal cell lines, at both the level of pathology and the level of viral gene expression. A reduced responsiveness to cell-cell contact inhibition and an increase in E6/E7 activity correlated closely with phenotype. Similar deregulation is likely to underlie the appearance of LSIL or HSIL soon after infection.

PMID:
22457518
PMCID:
PMC3372204
DOI:
10.1128/JVI.07069-11
[Indexed for MEDLINE]
Free PMC Article

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