New research has shown that a gene in human herpesvirus 8 (HHV8), a virus found in Kaposi's sarcoma (KS) tissues, may be involved in the transition of KS from slow growing to a state of rapid growth.
This work, by Dr. Michael Stürzl of the Institute for Molecular Virology, Neuherberg, Germany, and colleagues, is reported in the October 20 issue of the Journal of the National Cancer Institute.
KS occurs predominately in the skin, visceral organs, and lymph nodes, and often develops in people with acquired immunodeficiency virus (AIDS). DNA sequences from HHV8 have been identified in skin biopsies of KS lesions, and HHV8 infection appears to precede the onset of KS. However, the role that HHV8 plays in progression of KS is unclear. Because previous studies have identified genes (ORFK13, ORF72, and ORF73) in the HHV8 whose protein expressions may influence the progression of KS, the authors investigated these genes in KS and lymph node tissues.
Fourteen KS biopsy specimens (12 from AIDS-related KS lesions and two from classical KS lesions) from lesions in different stages of development were available for study, plus one lymph node infected by HHV8. The authors used an optimized in situ hybridization procedure to examine ORFK13-72-73 locus transcripts in HHV8-infected cells and in the lymph node. Apoptosis (programmed cell death) in KS lesions was also determined.
In summary, the authors report that the ORFK13-72-73 locus appears to be spliced differently in HHV8-infected cells in the KS lesions and in the lymph node. In addition, the ORFK13 gene sequences that encode the antiapoptotic protein v-FLIP are expressed at very low levels in early KS lesions, but this expression increases dramatically in late-stage lesions. This increase in expression of v-FLIP is associated with a reduction in apoptosis in KS lesions and may explain the transition from slow to rapid growth that is seen in later stages of KS development.
Editorial writer Gary Hayward, Ph.D., The Johns Hopkins School of Medicine, says that, while infection with the HHV8 does not by itself create a high risk of contracting KS, it is now almost certain that no cases of KS occur without the presence of HHV8 as the primary triggering agent. For AIDS patients infected with HHV8, the chance of developing KS within 10 years may be as high as 50%. The finding of Stürzl and others may lead to greater efforts to understand the basic fundamentals of KS and to develop antiviral and antineoplastic agents that can control KS.
Contact: Heinz-Joerg Haury, Germany, 49-89-3187-2460; fax 49-89-3187-3324. Editorial: Margorie Centofanti, Johns Hopkins, (410) 955-8725; fax (410) 955-4452.
Note: This memo to reporters is from the Journal staff and is not an official release of the National Cancer Institute (NCI) or Oxford University Press (OUP) nor does it reflect NCI or OUP policy. In addition, unless otherwise stated, all articles and items published in the Journal reflect the individual views of the authors and not necessarily the official points of view held by NCI, any other component of the U.S. government, OUP, or the organizations with which the authors are affiliated. Neither NCI nor any other component of the U.S. government nor OUP assumes any responsibility for the completeness of the articles or other items or the accuracy of the conclusions reached therein.
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