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J. Biol. Chem., Vol. 276, Issue 16, 13427-13432, April 20, 2001
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From the Departments of Human herpesvirus 8 (HHV8) is the primary viral
etiologic agent in Kaposi's sarcoma (KS). However, individuals dually
infected with both HHV8 and human immunodeficiency virus type 1 (HIV-1) show an enhanced prevalence of KS when compared with those singularly infected with HHV8. Host immune suppression conferred by HIV infection cannot wholly explain this increased presentation of KS. To better understand how HHV8 and HIV-1 might interact directly in the
pathogenesis of KS, we queried for potential regulatory interactions
between the two viruses. Here, we report that HHV8 and HIV-1
reciprocally up-regulate the gene expression of each other. We found
that the KIE2 immediate-early gene product of HHV8
interacted synergistically with Tat in activating expression from the
HIV-1 long terminal repeat. On the other hand, HIV-1 encoded Tat
and Vpr proteins increased intracellular HHV8-specific expression.
These results provide molecular insights correlating coinfection with
HHV8 and HIV-1 with an unusually high incidence of KS.
Reciprocal Regulatory Interaction between Human Herpesvirus 8 and
Human Immunodeficiency Virus Type 1*
§,¶,
,,
Pediatrics and
¶ Internal Medicine, National Taiwan University Hospital and
Division of Molecular and Genomic Medicine, National Health
Research Institutes, Taipei 100, Taiwan
*
This project was supported by a grant (NSC 88-2314-B002-139)
from National Science Council, Republic of China, a grant from the
Center for Disease Control, Department of Health, Taiwan, and a grant
from the China Medical College Hospital, Taichung, Taiwan.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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