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Journal of Virology, September 2002, p. 8729-8736, Vol. 76, No. 17
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.17.8729-8736.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Hemagglutinin Protein of Wild-Type Measles Virus Activates Toll-Like Receptor 2 Signaling

Karen Bieback,1 Egil Lien,2 Ingo M. Klagge,1 Elita Avota,1 Jürgen Schneider-Schaulies,1 W. Paul Duprex,3 Herrmann Wagner,4 Carsten J. Kirschning,4 Volker ter Meulen,1 and Sibylle Schneider-Schaulies1*

Institute for Virology and Immunobiology, University of Würzburg, D-97078 Würzburg,1 Institute for Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, Munich, Germany,4 University of Massachusetts Medical School, Worcester, Massachusetts 01605,2 School of Biochemistry, The Queen's University of Belfast, Belfast BT7 9BL, Northern Ireland, United Kingdom3

Received 22 March 2002/ Accepted 3 June 2002

Pattern recognition via Toll-like receptors (TLR) by antigen-presenting cells is an important element of innate immunity. We report that wild-type measles virus but not vaccine strains activate cells via both human and murine TLR2, and this is a property of the hemagglutinin (H) protein. The ability to activate cells via TLR2 by wild-type MV H protein is abolished by mutation of a single amino acid, asparagine at position 481 to tyrosine, as is found in attenuated strains, which is important for interaction with CD46, the receptor for these strains. TLR2 activation by MV wild-type H protein stimulates induction of proinflammatory cytokines such as interleukin-6 (IL-6) in human monocytic cells and surface expression of CD150, the receptor for all MV strains. Confirming the specificity of this interaction, wild-type H protein did not induce IL-6 release in macrophages from TLR2-/- mice. Thus, the unique property of MV wild-type strains to activate TLR2-dependent signals might essentially contribute not only to immune activation but also to viral spread and pathogenicity by upregulating the MV receptor on monocytes.

* Corresponding author. Mailing address: Institute for Virology and Immunobiology, University of Würzburg, Versbacher Str. 7, D-97078 Würzburg, Germany. Phone: 49-931-201-49895. Fax: 49-931-201-49553. E-mail: s-s-s{at}vim.uni-wuerzburg.de.

Journal of Virology, September 2002, p. 8729-8736, Vol. 76, No. 17
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.17.8729-8736.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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