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[Warts, viruses, cancer (author's transl)].
Annales De Dermatologie Et De Venereologie
|May 1, 1978
Summary
Human papillomavirus (HPV) in epidermodysplasia verruciformis (E.V.) may undergo cycles in skin cells, potentially leading to malignant transformation. Incorporating HPV DNA into the genome increases cancer risk, advising against mutagenic treatments.
Area of Science:
- Dermatology
- Virology
- Oncology
Background:
- Epidermodysplasia verruciformis (E.V.) involves cutaneous lesions caused by human papillomavirus (HPV).
- Malignant transformation of these lesions shares similarities with polyoma virus-induced changes.
- Understanding HPV's role in E.V. is crucial for managing associated risks.
Purpose of the Study:
- To compare malignant transformation in E.V. lesions with polyoma virus-induced changes.
- To elucidate the viral cycles and genetic mechanisms involved in HPV-related skin cancers.
- To provide guidance on managing HPV-induced lesions, particularly in E.V. patients.
Main Methods:
- Comparative analysis of HPV-induced E.V. lesions and polyoma virus models.
- Investigation of HPV's life cycle (lytic, transformant, abortive) in epidermal cells.
- Assessment of viral DNA integration and its impact on cellular processes and antigen production.
Main Results:
- HPV may undergo lytic, transformant, or abortive cycles in epidermal cells.
- Abortive cycles can increase DNA synthesis and lead to virus-coded cellular antigen production.
- Partial HPV DNA integration into the host genome enhances susceptibility to malignant transformation by other Papovaviruses.
Conclusions:
- HPV integration into the host genome is a key factor in malignant transformation of E.V. lesions.
- The presence of viral DNA increases cellular susceptibility to further oncogenic events.
- Mutagenic treatments like UV or X-ray irradiation are not recommended for managing HPV-induced lesions in E.V.