KERATOACANTHOMAS - HUMAN-PAPILLOMAVIRUS AND HERPES-SIMPLEX VIRUS-ASSOCIATED

Background A viral cause for keratoacanthoma has been postulated by ma ny investigators. Recently, some investigators reported the identifica tion of genital high risk human papilloma virus types 16 and 18 in ker atoacanthomas from transplant recipients. Observations We analysed by polymerase chain reaction biopsies of six multiple keratoacanthomas an d four solitary keratoacanthoma biopsies for the presence of the most common genital papilloma viruses, All keratoacanthomas included in the study had developed in skin areas exposed to sunlight. In addition, w e analysed 16 normal skin tissue biopsies, Six of these control tissue biopsies were from sun-exposed skin areas, while ID were from skin ar eas not exposed to sunlight. None of the patients enrolled in the stud y had clinical evidence of immunosuppression. As herpes simplex virus is associated to a variety of skin diseases and might co-operate with human papilloma virus in cervical cancer, the presence of this virus i n bioptic specimens was also addressed. Results DNA sequences from onc ogenic papilloma viruses type 16 and 18 were disclosed in two of four solitary keratoacanthomas, three of six multiple keratoacanthomas and four of six biopsies from sun-exposed normal skin. Non-oncogenic papil loma viruses (type 6 or 11) were detected only in one biopsy from a mu ltiple keratoacanthoma, and herpes simplex virus DNA was disclosed II one solitary keratoacanthoma, one multiple keratoacanthoma and one tis sue biopsy from sun-exposed skin. All specimens positive for herpes si mplex virus were co-infected with human papilloma virus type 16, but t his association was not statistically significant (Fisher's exact test ; P = 0.14). None of the tissue biopsies from sun-protected normal ski n was positive for these viruses. The difference of viral prevalence i n sun-exposed and non-exposed skin was statistically significant (P = 1.5 x 10(-3)). Conclusions In this study, human papilloma virus type 1 6 was detected with a high prevalence in keratoacanthomas and normal s kin from immunocompetent individuals. The different prevalence of vira l DNA in sun-exposed and non-exposed skin suggests that sunlight may f avour viral infection. The comparable prevalence of viral DNA in neopl astic and normal tissue from skin areas exposed to sunlight would indi cate that human papilloma virus infection occurred after the onset of neoplastic proliferation. In turn, the rapid growth of keratoacanthoma s and the high viral prevalence (50%) would imply a high overall rate of infection (and/or re-infection). The role of herpes simplex virus i n this cutaneous pathology in unclear. (C) 1997 Elsevier Science Irela nd B.V.