Abstract
Papillomaviruses are highly tissue-specific, and are characterized by a specific mode of interaction with the squamous epithelia they infect.1 It has been proposed that this interaction presents two successive steps that depend on the stage of differentiation of the host cell in the wart. In the basal germinal cells the viral replication is never observed. Based on the well-studied model of the papillomas induced by the Shope cottontail rabbit papillomavirus, it is most likely that the viral genome is present in the basal cells as a small number (10 to 50) of extrachromosomal copies.2,3 The viral messenger RNAs expressed correspond to nonstructural viral proteins, as yet unidentified, but most probably involved in the altered response of basal cells to the mechanisms regulating their mitotic rate and the size of the germinal cell population, thus resulting in the formation of a papilloma.4 Vegetative viral DNA replication is triggered upon the onset of the terminal differentiation process in the suprabasal layers, followed by the synthesis of viral structural proteins and the assembly of viral particles in more superficial layers.1,4
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