Date of this Version
Virology. 2010 September 30; 405(2): 342–351.
Anogenital cancers and head and neck cancers are causally-associated with infection by high-risk
human papillomavirus (HPV). The mechanism by which high-risk HPVs contribute to
oncogenesis is poorly understood. HPV16 encodes three genes (HPV16 E5, E6, and E7) that can
transform cells when expressed independently. HPV16 E6 and E7 have well-described roles
causing genomic instability and unregulated cell cycle progression. The role of HPV16 E5 in cell
transformation remains to be elucidated. Expression of HPV16 E5 results in enlarged, polyploid
nuclei that are dependent on the level and duration of HPV16 E5 expression. Live-cell imaging
data indicate these changes do not arise from cell-cell fusion or failed cytokinesis. The increase in
nuclear size is a continual process that requires DNA synthesis. We conclude HPV16 E5 produces
polyploid cells by endoreplication. These findings provide insight into how HPV16 E5 can
contribute to cell transformation.
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