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Journal of Virology, October 2005, p. 12944-12951, Vol. 79, No. 20
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.20.12944-12951.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Activation of Innate Defense against a Paramyxovirus Is Mediated by RIG-I and TLR7 and TLR8 in a Cell-Type-Specific Manner

Jesper Melchjorsen,1 Søren B. Jensen,1 Lene Malmgaard,1 Simon B. Rasmussen,1 Friedemann Weber,2 Andrew G. Bowie,3 Sampsa Matikainen,4 and Søren R. Paludan1*

Department of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark,1 Abteilung Virologie, Institut fur Medizinische Mikrobiologie und Hygiene, Universität Freiburg, Freiburg, Germany,2 Department of Biochemistry, Trinity College, Dublin, Ireland,3 Department of Microbiology, National Public Health Institute, Helsinki, Finland4

Received 7 June 2005/ Accepted 22 July 2005

Recognition of pathogens by the innate immune system is mediated by pattern recognition receptors (PRRs), which recognize specific molecular structures of the infectious agents and subsequently trigger expression of genes involved in host defense. Toll-like receptors (TLRs) represent a well-characterized class of membrane-bound PRRs, and the RNA helicase retinoic acid inducible gene I (RIG-I) has recently been described as a novel cytoplasmic PRR recognizing double-stranded RNA (dsRNA). Here we show that activation of signal transduction and induction of cytokine expression by the paramyxovirus Sendai virus is dependent on virus replication and involves PRRs in a cell-type-dependent manner. While nonimmune cells relied entirely on recognition of dsRNA through RIG-I for activation of an antiviral response, myeloid cells utilized both the single-stranded RNA sensing TLR7 and TLR8 and dsRNA-dependent mechanisms independent of RIG-I, TLR3, and dsRNA-activated protein kinase R to trigger this response. Therefore, there appears to be a large degree of cell-type specificity in the mechanisms used by the host to recognize infecting viruses.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, The Bartholin Building, University of Aarhus, DK-8000 Aarhus C, Denmark. Phone: (45) 8942 1766. Fax: (45) 8619 6128. E-mail: srp{at}microbiology.au.dk.

Journal of Virology, October 2005, p. 12944-12951, Vol. 79, No. 20
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.20.12944-12951.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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