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

Authors
Type
Published Article
Journal
Journal of Virology
1098-5514
Publisher
American Society for Microbiology
Publication Date
Volume
86
Issue
11
Pages
6358–6364
Identifiers
DOI: 10.1128/JVI.07069-11
PMID: 22457518
Source
Medline
License
Unknown

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.

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