© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 20, 1705-1707,
October 20, 1999
© 1999 Oxford University Press
EDITORIAL |
Human Herpesvirus 8 Latent-State Gene Expression and Apoptosis in Kaposi's Sarcoma Lesions
Correspondence to: Gary S. Hayward, Ph.D., Molecular Virology Laboratories, Departments of Oncology and of Pharmacology and Molecular Sciences, The Johns Hopkins School of Medicine, 725 N. Wolfe St., WBSB 317, Baltimore, MD 21205 (e-mail: ghayward@jhmi.edu).
The evidence that Kaposi's sarcoma (KS)-associated herpesvirus
(also known as human herpesvirus 8 [HHV8]) is the primary etiologic
agent of KS in both acquired immunodeficiency syndrome (AIDS) and
non-AIDS situations has been accumulating rapidly. Two recent articles,
one by Dupin et al. (1) and the other by Sturzl et al.
(2), which appears in this issue of the Journal, provide the
most compelling evidence yet for the almost universal presence of HHV8
and its latent-state gene products in the spindle-like tumor cells
characteristic of late-stage angiogenic nodular KS lesions. Although
previously known as only a very rare skin condition occurring primarily
in elderly Mediterranean Jewish men (classical KS) and in adolescent
males in the malaria belt in central Africa (endemic KS), KS has come
to sudden prominence since the early 1980s in the United States as one
of the original defining conditions of the AIDS epidemic
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