Abstract
THE human papillomaviruses (HPV) are associated specifically with epithelial lesions, ranging from benign warts to invasive carcinoma (for review, see refs 1, 2). The virus encodes three late proteins, which are produced only in terminally differentiating keratinocytes, two of which are structural components of the virion3. The third, E1–E4, is derived primarily from the E4 open reading frame, which represents a region of maximal divergence between different HPV types4,5. E1–E4 does not seem to be a component of the virus particle or to be needed for transformation in vitro6,7, but accumulates in the cytoplasm5,8–10, where in certain benign lesions it can comprise 20–30% of total cell protein4,10. We show here that expression of the HPV-16 E1–E4 protein in human keratinocytes (the natural host cell for HPV infection) results in the total collapse of the cytokeratin matrix. Tubulin and actin networks are unaffected by E1–E4, as are the nuclear lamins.
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Doorbar, J., Ely, S., Sterling, J. et al. Specific interaction between HPV-16 E1–E4 and cytokeratins results in collapse of the epithelial cell intermediate filament network. Nature 352, 824–827 (1991). https://doi.org/10.1038/352824a0
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DOI: https://doi.org/10.1038/352824a0
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