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Journal of Virology, November 2007, p. 12091-12096, Vol. 81, No. 21
0022-538X/07/$08.00+0 doi:10.1128/JVI.01264-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Virology, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582,1 Department of Virology 3, National Institute of Infectious Diseases, Musashi-Murayama, Tokyo 208-0011, Japan2
Received 11 June 2007/ Accepted 15 August 2007
Measles virus (MV) propagates mainly in lymphoid organs throughout the body and produces syncytia by using signaling lymphocyte activation molecule (SLAM) as a receptor. MV also spreads in SLAM-negative epithelial tissues by unknown mechanisms. Ubiquitously expressed CD46 functions as another receptor for vaccine strains of MV but not for wild-type strains. We here show that MV grows and produces syncytia efficiently in a human lung adenocarcinoma cell line via a SLAM- and CD46-independent mechanism using a novel receptor-binding site on the hemagglutinin protein. This infection model could advance our understanding of MV infection of SLAM-negative epithelial cells and tissues.
Published ahead of print on 22 August 2007.
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