Doorbar J, Ely S, Sterling J, McLean C, Crawford L
Department of Pathology, University of Cambridge, UK.
Nature. 1991 Aug 29;352(6338):824-7. doi: 10.1038/352824a0.
The human papillomaviruses (HPV) are associated specifically with epithelial lesions, ranging from benign warts to invasive carcinoma. The virus encodes three late proteins, which are produced only in terminally differentiating keratinocytes, two of which are structural components of the virion. The third, E1-E4, is derived primarily from the E4 open reading frame, which represents a region of maximal divergence between different HPV types. E1-E4 does not seem to be a component of the virus particle or to be needed for transformation in vitro, but accumulates in the cytoplasm, where in certain benign lesions it can comprise 20-30% of total cell protein. 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.
人乳头瘤病毒（HPV）与上皮病变密切相关，范围从良性疣到浸润性癌。该病毒编码三种晚期蛋白，仅在终末分化的角质形成细胞中产生，其中两种是病毒体的结构成分。第三种，E1-E4，主要来源于E4开放阅读框，它代表了不同HPV类型之间差异最大的区域。E1-E4似乎不是病毒颗粒的组成成分，在体外转化过程中也不需要，但会在细胞质中积累，在某些良性病变中，它可占细胞总蛋白的20%-30%。我们在此表明，HPV-16 E1-E4蛋白在人角质形成细胞（HPV感染的天然宿主细胞）中的表达会导致细胞角蛋白基质完全崩溃。微管蛋白和肌动蛋白网络不受E1-E4影响，核纤层蛋白也是如此。
