This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pulmanausahakul, R.
Right arrow Articles by Dietzschold, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pulmanausahakul, R.
Right arrow Articles by Dietzschold, B.

 Previous Article  |  Next Article 

Journal of Virology, March 2008, p. 2330-2338, Vol. 82, No. 5
0022-538X/08/$08.00+0     doi:10.1128/JVI.02327-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

The Glycoprotein and the Matrix Protein of Rabies Virus Affect Pathogenicity by Regulating Viral Replication and Facilitating Cell-to-Cell Spread{triangledown}

Rojjanaporn Pulmanausahakul,1 Jianwei Li,1 Matthias J. Schnell,1,2 and Bernhard Dietzschold1,2*

Department of Microbiology and Immunology,1 Jefferson Vaccine Center, Thomas Jefferson University, Philadelphia, Pennsylvania2

Received 26 October 2007/ Accepted 12 December 2007

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 roles 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 the SN strain bearing the RV G from the pathogenic SB strain. Moreover, the pathogenicity was further increased when both G and M from SB were introduced into SN. Interestingly, the replacement of the G or M gene 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 gene was replaced. Together, these data indicate that both G and M play an important role in RV pathogenesis by regulating virus replication and facilitating cell-to-cell spread.

* Corresponding author. Mailing address: 233 South 10th Street, BLSB 533, Philadelphia, PA 19107-5541. Phone: (215) 503-4692. Fax: (215) 503-5393. E-mail: bernhard.dietzschold{at}jefferson.edu

{triangledown} Published ahead of print on 19 December 2007.

Journal of Virology, March 2008, p. 2330-2338, Vol. 82, No. 5
0022-538X/08/$08.00+0     doi:10.1128/JVI.02327-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Anderson, D. E., von Messling, V. (2008). Region between the Canine Distemper Virus M and F Genes Modulates Virulence by Controlling Fusion Protein Expression. J. Virol. 82: 10510-10518 [Abstract] [Full Text]  
  • Wirblich, C., Tan, G. S., Papaneri, A., Godlewski, P. J., Orenstein, J. M., Harty, R. N., Schnell, M. J. (2008). PPEY Motif within the Rabies Virus (RV) Matrix Protein Is Essential for Efficient Virion Release and RV Pathogenicity. J. Virol. 82: 9730-9738 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»