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Journal of Virology, July 2002, p. 6743-6749, Vol. 76, No. 13
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.13.6743-6749.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

SLAM (CD150)-Independent Measles Virus Entry as Revealed by Recombinant Virus Expressing Green Fluorescent Protein

Koji Hashimoto,1 Nobuyuki Ono,1 Hironobu Tatsuo,1 Hiroko Minagawa,1 Makoto Takeda,2 Kaoru Takeuchi,2 and Yusuke Yanagi1*

Department of Virology, Faculty of Medicine, Kyushu University, Fukuoka 812-8582,1 Department of Virus Diseases and Vaccine Control, National Institute of Infectious Diseases, Musashi-murayama, Tokyo 208-0011, Japan2

Received 8 January 2002/ Accepted 4 April 2002

Wild-type measles virus (MV) strains use human signaling lymphocyte activation molecule (SLAM) as a cellular receptor, while vaccine strains such as the Edmonston strain can use both SLAM and CD46 as receptors. Although the expression of SLAM is restricted to cells of the immune system (lymphocytes, dendritic cells, and monocytes), histopathological studies with humans and experimentally infected monkeys have shown that MV also infects SLAM-negative cells, including epithelial, endothelial, and neuronal cells. In an attempt to explain these findings, we produced the enhanced green fluorescent protein (EGFP)-expressing recombinant MV (IC323-EGFP) based on the wild-type IC-B strain. IC323-EGFP showed almost the same growth kinetics as the parental recombinant MV and produced large syncytia exhibiting green autofluorescence in SLAM-positive cells. Interestingly, all SLAM-negative cell lines examined also showed green autofluorescence after infection with IC323-EGFP, although the virus hardly spread from the originally infected individual cells and thus did not induce syncytia. When the number of EGFP-expressing cells after infection was taken as an indicator, the infectivities of IC323-EGFP for SLAM-negative cells were 2 to 3 logs lower than those for SLAM-positive cells. Anti-MV hemagglutinin antibody or fusion block peptide, but not anti-CD46 antibody, blocked IC323-EGFP infection of SLAM-negative cells. This infection occurred under conditions in which entry via endocytosis was inhibited. These results indicate that MV can infect a variety of cells, albeit with a low efficiency, by using an as yet unidentified receptor(s) other than SLAM or CD46, in part explaining the observed MV infection of SLAM-negative cells in vivo.

* Corresponding author. Mailing address: Department of Virology, Faculty of Medicine, Kyushu University, Fukuoka 812-8582, Japan. Phone: 81-92-642-6135. Fax: 81-92-642-6140. E-mail: yyanagi{at}virology.med.kyushu-u.ac.jp.

Journal of Virology, July 2002, p. 6743-6749, Vol. 76, No. 13
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.13.6743-6749.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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