The Journal of Experimental Medicine
Aegean Conferences: 2009 Conferences
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Published 2 August 2004. doi:10.1084/jem.20031881
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 3, 391-398
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Brief Definitive Report

 Highly Selective Escape from KSHV-mediated Host mRNA Shutoff and Its Implications for Viral Pathogenesis

Britt Glaunsinger and Don Ganem

Howard Hughes Medical Institute, Department of Microbiology, and Department of Medicine, University of California, San Francisco, San Francisco, CA 94143

Address correspondence to Don Ganem, Howard Hughes Medical Institute, Dept. of Microbiology, and Dept. of Medicine, University of California, San Francisco, 513 Parnassus Ave., Box 0414, San Francisco, CA 94143. Phone: (415) 476-2826; Fax: (415) 476-0939; email: ganem{at}cgl.ucsf.edu

During Kaposi's sarcoma (KS)–associated herpesvirus (KSHV) lytic infection, many virus-encoded signaling molecules (e.g., viral G protein–coupled receptor [vGPCR]) are produced that can induce host gene expression in transiently transfected cells, and roles for such induced host genes have been posited in KS pathogenesis. However, we have recently found that host gene expression is strongly inhibited by 10–12 h after lytic reactivation of KSHV, raising the question of whether and to what extent de novo host gene expression induced by viral signaling molecules can proceed during the lytic cycle. Here, we show by microarray analysis that expression of most vGPCR target genes is drastically curtailed by this host shutoff. However, rare cellular genes can escape the host shutoff and are potently up-regulated during lytic KSHV growth. Prominent among these is human interleukin-6, whose striking induction may contribute to the overexpression of this cytokine in several disease states linked to KSHV infection.

Key Words: KSHV • DNA array • GPCR • Castleman's disease • herpesvirus • Kaposi's sarcoma


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