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Journal of Virology, September 2004, p. 9336-9342, Vol. 78, No. 17
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.17.9336-9342.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Tumorigenesis by Human Herpesvirus 8 vGPCR Is Accelerated by Human Immuodeficiency Virus Type 1 Tat

Hong-Guang Guo, Shibani Pati, Mariola Sadowska, Man Charurat, and Marvin Reitz*

Institute of Human Virology, University of Maryland Biotechnology Institute, Baltimore, Maryland

Received 24 October 2003/ Accepted 30 April 2004

Human herpesvirus 8 (HHV-8), also called Kaposi's sarcoma (KS) herpesvirus, can cause KS but is inefficient. Untreated human immunodeficiency virus type 1 (HIV-1) coinfection is a powerful risk factor. The HHV-8 chemokine receptor, vGPCR (ORF74), activates NF-{kappa}B and NF-AT, and their levels of activation are synergistically increased by HIV-1 Tat. Transgenic vGPCR mice develop KS-like tumors. A cell line derived from one such tumor expresses vGPCR and forms tumors in nude mice. Here we show that transfection of DNA encoding HIV-1 tat (but not a transactivation-defective mutant) into these tumor cells increases NF-{kappa}B and NF-AT activation levels and accelerates tumor formation. Tumorigenesis was also accelerated when Tat DNA was transfected into normal cells and the transfected cells were mixed with the tumor cells and injected into a single site. Tumorigenesis was also increased when the two cell types were injected at separate sites, suggesting that tumorigenesis is accelerated by Tat through soluble factors.

* Corresponding author. Mailing address: University of Maryland Biotechnology Institute, Institute of Human Virology, 725 W. Lombard St., Baltimore, MD 21201. Phone: (410) 706-4679. Fax: (410) 706-4694. E-mail: reitz{at}umbi.umd.edu.

Journal of Virology, September 2004, p. 9336-9342, Vol. 78, No. 17
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.17.9336-9342.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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