| Literature DB >> 11857356 |
Rastine Merat1, Ali Amara, Celeste Lebbe, Hugues de The, Patrice Morel, Ali Saib.
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus etiologically linked to primary effusion lymphoma (PEL), to a subset of multicentric Castleman's disease and to Kaposi's sarcoma (KS), the most common neoplasm associated with AIDS. Among KSHV-infected individuals, the risk of KS is much higher in those with human immunodeficiency-1 (HIV-1) infection than among those with other types of immunosuppression, suggesting a direct action of HIV-1 on KSHV replication. We show in our report that BC-3 cells, a chronically KSHV-infected B-cell line of a PEL origin, are permissive to HIV-1, offering a new tool for studying the interactions between these 2 viruses. In these cells, HIV-1 infection leads to reactivation of latent KSHV genomes, as demonstrated by the expression of KSHV lytic viral mRNAs. Although recombinant HIV-1 gp120 fails to enhance herpesvirus expression, transient transfection of the HIV-1 trans-activator Tat suffices to reactivate latent KSHV. By showing that HIV-1 infection directly reactivates latent KSHV, our results suggest a direct role of HIV-1 in the onset of KS in coinfected individuals. Copyright 2001 Wiley-Liss, Inc.Entities:
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Year: 2002 PMID: 11857356 DOI: 10.1002/ijc.10086
Source DB: PubMed Journal: Int J Cancer ISSN: 0020-7136 Impact factor: 7.396