HUMAN HERPESVIRUS-8 (KAPOSIS-SARCOMA-ASSOCIATED HERPESVIRUS) DNA IN KAPOSIS-SARCOMA LESIONS, AIDS KAPOSIS-SARCOMA CELL-LINES, ENDOTHELIAL KAPOSIS-SARCOMA SIMULATORS, AND THE SKIN OF IMMUNOSUPPRESSED PATIENTS

We used the polymerase chain reaction on 63 tissue specimens of histol ogically staged classic Kaposi's sarcoma (KS) from 40 patients, 14 spe cimens from 14 acquired immune deficiency syndrome (AIDS)-KS cases (al l from the same geographic area over a 10-year period), and peripheral blood mononuclear cells from 1 of the non-AIDS KS patients to amplify a specific 210-bp genomic sequence of the newly discovered KS-associa ted herpesvirus (KSHV). Also tested were 86 benign and malignant endot helial lesions, which potentially simulated each KS histological stage and were further matched by age approximation and by sex with a class ical KS specimen. The lesions included hemangioma, lymphangioma, pyoge nic granuloma, and angiosarcoma. KSHV was also sought in multiple well characterized vascular endothelial cell lines from AIDS-KS lesions an d in 20 mainly cutaneous benign and malignant lesions from 15 immunosu ppressed transplant patients. Overall, 92% of KS tissue specimens, rep resenting 88% of classical KS and 100% of AIDS-KS patients, and in add ition the sample of peripheral blood mononuclear cell DNA, were positi ve as visualized on ethidium bromide gels and confirmed by Southers bl ot hybridization (only 1 case was negative on gel visualization but po sitive off Southern blot), thus confirming the close association of KS HV with KS of different clinical forms. None of the various other endo thelial lesions, skin lesions in immunosuppressed patients, or AIDS-KS endothelial cell lines contained amplifiable KSHV DNA, which indicate s that reactivation of KSHV is not present in the skin lesions of immu nosuppressed patients and probably is not a ubiquitous agent that seco ndarily infects proliferative, endothelium, The absence of amplifiable virus DNA in the cultured endothelium of KS suggests that the stimulu s for angioproliferation originates in another host cell or tinder con ditions not reproduced in culture. The polymerase chain reaction is a specific and sensitive means of verifying KS in the differential diagn osis of angioproliferative lesions.