HIV-1 infection of primary effusion lymphoma cell line triggers Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation

✍ Scribed by Rastine Merat; Ali Amara; Celeste Lebbe; Hugues de The; Patrice Morel; Ali Saib

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: French
• Weight: 238 KB
• Volume: 97
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.10086

✦ Synopsis

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. © 2001 Wiley‐Liss, Inc.