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Blood, 1 August 2004, Vol. 104, No. 3, pp. 810-814.
Prepublished online as a Blood First Edition Paper on April 13, 2004April 8, 2004; DOI 10.1182/blood-2003-07-2533.


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Submitted July 25, 2003
Accepted March 26, 2004

HIV-1 Tat enhances KSHV infectivity

Yoshiyasu Aoki* and Tosato Giovanna

Experimental Transplantation and Immunology Branch, National Cancer Institute, Bethesda, MD, USA

* Corresponding author; email: aokiy{at}mail.nih.gov.

The high frequency of Kaposi's sarcoma (KS) in immunodeficiency states, particularly in patients with AIDS, has been attributed to increased replication of KS-associated herpesvirus (KSHV), a necessary cofactor for KS development. However, experimental KSHV infection of endothelial lineage cells that compose KS lesions has been difficult even in the absence of immune cells. Here we show that HIV-1 Tat protein can directly promote KSHV transmission. Full-length HIV-1 Tat and a 13-amino-acid peptide corresponding to the basic region of Tat specifically enhances the entry of KSHV into endothelial and other cells, presenting evidence for an active role of HIV-1 in the development of KSHV-associated diseases. These results can explain why AIDS-KS is more frequent and clinically more aggressive than KS in other immunodeficiency states.


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