Human papillomavirus causes: Difference between revisions

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Revision as of 15:05, 14 October 2016

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Aysha Anwar, M.B.B.S [2]

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 ==Overview==
-== HPV Life-cycle ==
-The HPV life-cycle strictly follows the differentiation program of the host [[keratinocyte]]. It is thought that the HPV virion infects epithelial tissues through micro-abrasions, whereby, the virion associates with putative receptors such as alpha integrins and laminins, leading to entry of the virions into basal epithelial cells through clathrin-mediated endocytosis and/or caveolin-mediated endocytosis depending on the type of HPV. At this point, the viral genome is transported to the nucleus by unknown mechanisms and establishes itself at a copy number between 10-200 viral genomes per cell. A sophisticated transcriptional cascade then occurs as the host keratinocyte begins to divide and become increasingly differentiated in the upper layers of the epithelium. The viral oncogenes, E6 and E7, are thought to modify the cell cycle so as to retain the differentiating host keratinocyte in a state that is amiable to the amplification of viral genome replication and consequent late gene expression. In the upper layers of the host epithelium, the late genes L1 and L2 are transcribed/translated and serve as structural proteins which encapsidate the amplified viral genomes. Virions can then be sloughed off in the dead squames of the host epithelium and the viral life-cycle continues.
 ==References==