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Herbert Pfister, MD

Arch Dermatol. 1987;123(11):1469-1470.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

At least 45 different human papillomavirus (HPV) types are presently known, which induce epithelial tumors of the skin or mucosa.¹ The majority of the warts, papillomas, leukoplakias, or hyperplasias are benign, but some lesions, particularly dysplasias of the cervix uteri, macules of patients with epidermodysplasia verruciformis (EV), and laryngeal papillomas in adults, may progress to squamous cell carcinomas. Infection by HPV elicits humoral and cellular immune mechanisms against virus particles and tumor tissue,^2,3 which trigger tumor regression and leave the host immune to reinfection.

The incidence of some HPV types appears rather unaffected by the immune status of the patient, while susceptibility to other types depends more or less on an impaired immune system. Infections by HPV 2, 3, 4, and 10, for example, are considerably favored by a compromised immune system, which is reflected by the frequent occurrence in immunosuppressed allograft recipients.^4-6 . . . [Full Text PDF of this Article]

Author Affiliations
Institut für Klinische und Molekulare Virologie Universität Erlangen-Nürnberg Erlangen, West Germany

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