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J. Virol. doi:10.1128/JVI.02327-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The glycoprotein and matrix protein of rabies virus affect pathogenicity by regulating viral replication and facilitating cell-to-cell spread

Department of Microbiology and Immunology, Jefferson Vaccine Center, Thomas Jefferson University, Philadelphia, Pennsylvania

^* To whom correspondence should be addressed. Email: bernhard.dietzschold{at}jefferson.edu.

	Abstract

While the glycoprotein (G) of rabies virus (RV) is known to play a predominant role in the pathogenesis of rabies, the function of the RV matrix protein (M) in RV pathogenicity is not completely clear. To further investigate the role of these proteins in viral pathogenicity, we constructed chimeric recombinant viruses by exchanging the G and M genes of the attenuated SN strain with those of the highly pathogenic SB strain. Infection of mice with these chimeric viruses revealed a significant increase in the pathogenicity of SN parental strain bearing the RV G from the pathogenic SB strain. Moreover, the pathogenicity was further increased when both the G and M proteins from SB were introduced into SN. Interestingly, replacement of the G or M or both in SN by the corresponding genes of SB was associated with a significant decrease in the rate of viral replication and viral RNA synthesis. In addition, a chimeric SN virus bearing both the M and G genes from SB exhibited more efficient cell-to-cell spread than a chimeric SN virus in which only the G was replaced. Together these data indicate that both the G and M proteins play an important role in RV pathogenesis by regulating virus replication and facilitating cell-to-cell spread.

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