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Journal of Virology, May 2000, p. 4139-4145, Vol. 74, No. 9
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Virus Entry Is a Major Determinant of Cell Tropism of Edmonston and Wild-Type Strains of Measles Virus as Revealed by Vesicular Stomatitis Virus Pseudotypes Bearing Their Envelope Proteins

Hironobu Tatsuo,1 Kazu Okuma,1 Kotaro Tanaka,1 Nobuyiki Ono,1 Hiroko Minagawa,1 Akemi Takade,2 Yoshiharu Matsuura,3 and Yusuke Yanagi1,*

Department of Virology1 and Department of Bacteriology,2 Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, and Department of Virology II, National Institute of Infectious Diseases, Tokyo 162-8640,3 Japan

Received 6 December 1999/Accepted 4 February 2000

The Edmonston strain of measles virus (MV) that utilizes the human CD46 as the cellular receptor produced cytopathic effects (CPE) in all of the primate cell lines examined. In contrast, the wild-type MV strains isolated in a marmoset B-cell line B95a (the KA and Ichinose strains) replicated and produced CPE in some but not all of the primate lymphoid cell lines. To determine the mechanism underlying this difference in cell tropism, we used a recently developed recombinant vesicular stomatitis virus (VSV) containing as a reporter the green fluorescent protein gene in lieu of the VSV G protein gene (VSVDelta G*). MV glycoproteins were efficiently incorporated into VSVDelta G*, producing the VSV pseudotypes. VSVDelta G* complemented with VSV G protein efficiently infected all of the cell lines tested. The VSV pseudotype bearing the Edmonston hemagglutinin (H) and fusion (F) protein (VSVDelta G*-EdHF) infected all cell lines in which the Edmonston strain caused CPE, including the rodent cell lines to which the human CD46 gene was stably transfected. The pseudotype bearing the wild-type KA H protein and Edmonston F protein (VSVDelta G*-KAHF) infected all lymphoid cell lines in which the wild-type MV strains caused CPE as efficiently as VSVDelta G*-EdHF, but it did not infect any of the cell lines resistant to infection with the KA strain. The results indicate that the difference in cell tropism between these MV strains was largely determined by virus entry, in which the H proteins of respective MV strains play a decisive role.

* Corresponding author. Mailing address: Department of Virology, Graduate School of Medical Sciences, 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, May 2000, p. 4139-4145, Vol. 74, No. 9
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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