A study for the molecular mechanisms of HPV-type specific cytopathogenic effect.

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We have established an experimental system which can evaluate the requirement of any viral gene of interest in the viral life cycle by supplying and deleting exogenous expression of the gene and demonstrated that E1 is entirely dispensable for maintenance replication of the HPV16 genome in human keratinocytes. Thus, inhibition of E1 may not be able to eliminate the viral genome from the basal cell layer. The rationale for development of E1 inhibitors as anti-HPV drugs may be more restricted than formerly envisaged.HPV 126, isolated and characterized in the present study, is a novel type of genus gamma papillomavirus and associated with flat wart- or EV-related tinea versicolor-like clinical features: histological ICBs as with other genus gamma papillomaviruses; and immunohistochemical expression of Ki-67 and p53 in characteristic manner not typical for benign cutaneous warts.