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Glycobiology Advance Access originally published online on April 6, 2009
Glycobiology 2009 19(7):776-788; doi:10.1093/glycob/cwp050
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© The Author 2009. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Activation of host antiviral RNA-sensing factors necessary for herpes simplex virus type 1-activated transcription of host cell fucosyltransferase genes FUT3, FUT5, and FUT6 and subsequent expression of sLex in virus-infected cells

Rickard Nordén2, Kristina Nyström2,3 and Sigvard Olofsson1,2

2 Department of Virology, University of Gothenburg, Gothenburg, Sweden
3 INSERM U892, Université de Nantes, Nantes, France

1 To whom correspondence should be addressed: Tel: +46-31-342-46-59; Fax: +46-31-82-70-32; e-mail: sigvard.olofsson{at}microbio.gu.se

Received on February 24, 2009; revised on March 23, 2009; accepted on March 30, 2009

Herpes simplex virus type 1 (HSV-1) induces expression of a selectin receptor, the carbohydrate epitope sialyl Lewis X (sLex), at the surface of infected cells. The molecular background to this phenomenon is that a viral immediate early RNA interacts with as yet unidentified host factors, eventually resulting in transcription of three dormant host fucosyltransferase genes (FUT3, FUT5, and FUT6), whose gene products are rate-limiting for synthesis of sLex. The aim of the present study was to define the immediate targets for the viral RNA in this process. We found that the Protein Kinase R (PKR) inhibitors 2-aminopurine (2-AP) and C16 inhibited FUT3, FUT5, and FUT6 expression as well as HSV-1-induced expression of sLex, indicating a primary role of PKR as a viral RNA target. The PKR-dependent activation of the FUT genes seemed neither to involve PKR effects on translation nor to involve NF-{kappa}B- or JNK-dependent activation. IMD-0354, known as an inhibitor of the NF-{kappa}B-activating factor IKK-2, induced FUT transcription via a novel IKK-2-independent mechanism, irrespective of whether the cells were virus-infected or not. Altogether, the results suggested that PKR is the primary target for HSV-1 early RNA during induction of FUT3, FUT5, and FUT6, and that the subsequent steps in the transcriptional activation of these host genes involve a hitherto unknown IMD-0354, yet IKK-2-independent, pathway.

Key words: dsRNA / ICP0 / IMD-0354 / PKR / Selectin


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