Background Herpesvirus-like DNA sequences have recently beenfound in lesions from patients with Kaposi's sarcoma and theacquired immunodeficiency syndrome (AIDS). It is not known whetherthese sequences are also present in classic Kaposi's sarcomaor in the Kaposi's sarcoma that occurs in homosexual men whoare seronegative for the human immunodeficiency virus (HIV).
Methods We analyzed DNA in tissue samples from patients withAIDS-associated Kaposi's sarcoma, patients with classic Kaposi'ssarcoma, and HIV-seronegative homosexual men with Kaposi's sarcoma.We also analyzed DNA in samples of uninvolved tissue from thesepatients and in control tissue from healthy subjects. All sampleswere tested blindly by polymerase chain reaction (PCR) withspecific primers to amplify KS330233, a herpesvirus-like DNAsequence.
Results The KS330233 PCR product was found in 20 of 21 tissuesamples (95 percent) from the patients with Kaposi's sarcoma,including 10 of the 11 samples from the patients with AIDS-associatedKaposi's sarcoma, all 6 samples from the patients with classicKaposi's sarcoma, and all 4 samples from the HIV-negative homosexualmen with Kaposi's sarcoma. Only 1 of the 21 control samples(5 percent) was positive (odds ratio, 400; 95 percent confidenceinterval, 19 to 17,300). Of the 14 samples of uninvolved skinfrom the patients with Kaposi's sarcoma, 3 were positive forKS330233. Representative PCR-product sequences were more than98 percent identical for the three types of Kaposi's sarcoma,suggesting that all three are caused by the same agent.
Conclusions The same herpesvirus-like DNA sequences are presentin AIDS-associated Kaposi's sarcoma, classic Kaposi's sarcoma,and the Kaposi's sarcoma that occurs in HIV-negative homosexualmen. Therefore, this presumably new human herpesvirus is notsolely an opportunistic infection in patients with AIDS, andthe three forms of Kaposi's sarcoma may be caused by the sameinfectious agent.
Source Information
From the Division of Epidemiology, School of Public Health (P.S.M.), and the Department of Pathology, College of Physicians and Surgeons (Y.C.), Columbia University, New York. Tissue DNA specimens were prepared and provided by Dr. Yao-Qi Huang, Dr. Jian J. Li, and Dr. Alvin Friedman-Kien of the Departments of Microbiology and Dermatology, New York University School of Medicine, New York.
Address reprint requests to Dr. Moore at the Division of Epidemiology, PH18, Columbia University, 630 W. 168th St., New York, NY 10032.
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