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Journal of Virology, August 2005, p. 10376-10385, Vol. 79, No. 16
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.16.10376-10385.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Early Alpha/Beta Interferon Production by Myeloid Dendritic Cells in Response to UV-Inactivated Virus Requires Viral Entry and Interferon Regulatory Factor 3 but Not MyD88

Åsa S. Hidmark,1 Gerald M. McInerney,1 Eva K. L. Nordström,1,2 Iyadh Douagi,1,2 Kristen M. Werner,1 Peter Liljeström,1,2 and Gunilla B. Karlsson Hedestam1,2*

Microbiology and Tumor Biology Center, Karolinska Institutet, SE-171 77 Stockholm, Sweden,1 Section of Vaccine Research, Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden2

Received 9 February 2005/ Accepted 5 May 2005

Alpha/beta interferons (IFN-{alpha}/ß) are key mediators of innate immunity and important modulators of adaptive immunity. The mechanisms by which IFN-{alpha}/ß are induced are becoming increasingly well understood. Recent studies showed that Toll-like receptors 7 and 8 expressed by plasmacytoid dendritic cells (pDCs) mediate the endosomal recognition of incoming viral RNA genomes, a process which requires myeloid differentiation factor 88 (MyD88). Here we investigate the requirements for virus-induced IFN-{alpha}/ß production in cultures of bone marrow-derived murine myeloid DCs (mDCs). Using recombinant Semliki Forest virus blocked at different steps in the viral life cycle, we show that replication-defective virus induced IFN-{alpha}/ß in mDCs while fusion-defective virus did not induce IFN-{alpha}/ß. The response to replication-defective virus was largely intact in MyD88–/– mDC cultures but was severely reduced in mDC cultures from mice lacking IFN regulatory factor 3. Our observations suggest that mDCs respond to incoming virus via a pathway that differs from the fusion-independent, MyD88-mediated endosomal pathway described for the induction of IFN-{alpha}/ß in pDCs. We propose that events during or downstream of viral fusion, but prior to replication, can activate IFN-{alpha}/ß in mDCs. Thus, mDCs may contribute to the antiviral response activated by the immune system at early time points after infection.

* Corresponding author. Mailing address: Microbiology and Tumor Biology Center, Karolinska Institutet, Box 280, S-171 77 Stockholm, Sweden. Phone: 46-8-457-2568. Fax: 46-8-310848. E-mail: Nilla.Karlsson{at}mtc.ki.se.

Journal of Virology, August 2005, p. 10376-10385, Vol. 79, No. 16
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.16.10376-10385.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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