Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 200, Issue 3, Pages 391-398Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20031881
Keywords
KSHV; DNA array; GPCR; Castleman's disease; herpesvirus; Kaposi's sarcoma
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During Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) lyric 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 lyric 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.
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