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 Welstead, G. G.
Right arrow Articles by Richardson, C. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Welstead, G. G.
Right arrow Articles by Richardson, C. D.

 Previous Article  |  Next Article 

Journal of Virology, September 2004, p. 9666-9674, Vol. 78, No. 18
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.18.9666-9674.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Mechanism of CD150 (SLAM) Down Regulation from the Host Cell Surface by Measles Virus Hemagglutinin Protein

G. Grant Welstead, Eric C. Hsu, Caterina Iorio, Shelly Bolotin, and Christopher D. Richardson*

Department of Medical Biophysics, University of Toronto, and Ontario Cancer Institute, Toronto, Canada

Received 25 March 2004/ Accepted 10 May 2004

Measles virus has been reported to enter host cells via either of two cellular receptors, CD46 and CD150 (SLAM). CD46 is found on most cells of higher primates, while SLAM is expressed on activated B, T, and dendritic cells and is an important regulatory molecule of the immune system. Previous reports have shown that measles virus can down regulate expression of its two cellular receptors on the host cell surface during infection. In this study, the process of down regulation of SLAM by measles virus was investigated. We demonstrated that expression of the hemagglutinin (H) protein of measles virus was sufficient for down regulation. Our studies provided evidence that interactions between H and SLAM in the endoplasmic reticulum (ER) can promote the down regulation of SLAM but not CD46. In addition, we demonstrated that interactions between H and SLAM at the host cell surface can also contribute to SLAM down regulation. These results indicate that two mechanisms involving either intracellular interactions between H and SLAM in the ER or receptor-mediated binding to H at the surfaces of host cells can lead to the down regulation of SLAM during measles virus infection.


* Corresponding author. Mailing address: Ontario Cancer Institute, 620 University Ave., Suite 706, Toronto, Ontario, Canada M5G 2C1. Phone: (416) 946-2849. Fax: (416) 204-2278. E-mail: chrisr{at}uhnres.utoronto.ca.


Journal of Virology, September 2004, p. 9666-9674, Vol. 78, No. 18
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.18.9666-9674.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Sawatsky, B., Grolla, A., Kuzenko, N., Weingartl, H., Czub, M. (2007). Inhibition of henipavirus infection by Nipah virus attachment glycoprotein occurs without cell-surface downregulation of ephrin-B2 or ephrin-B3. J. Gen. Virol. 88: 582-591 [Abstract] [Full Text]  
  • Welstead, G. G., Iorio, C., Draker, R., Bayani, J., Squire, J., Vongpunsawad, S., Cattaneo, R., Richardson, C. D. (2005). Measles virus replication in lymphatic cells and organs of CD150 (SLAM) transgenic mice. Proc. Natl. Acad. Sci. USA 102: 16415-16420 [Abstract] [Full Text]