JVI Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 Katayama, Y.
Right arrow Articles by Wong, T. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Katayama, Y.
Right arrow Articles by Wong, T. C.

 Previous Article  |  Next Article 

Journal of Virology, February 2000, p. 1252-1257, Vol. 74, No. 3
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Human Receptor for Measles Virus (CD46) Enhances Nitric Oxide Production and Restricts Virus Replication in Mouse Macrophages by Modulating Production of Alpha/Beta Interferon

Yuko Katayama,dagger Akiko Hirano, and Timothy C. Wong*

Department of Microbiology, University of Washington School of Medicine, Seattle, Washington 98195

Received 19 July 1999/Accepted 21 October 1999

Complement regulatory protein CD46 is a human cell receptor for measles virus (MV). In this study, we investigated why mouse macrophages expressing human CD46 restricted MV replication and produced higher levels of nitric oxide (NO) in response to MV and gamma interferon (IFN-gamma ). Treatment of MV-infected CD46-expressing mouse macrophages with antibodies against IFN-alpha /beta blocked NO production. Antibodies against IFN-alpha /beta also inhibited the augmenting effect of MV on IFN-gamma -induced NO production in CD46-expressing mouse macrophages. These antibodies did not affect NO production induced by IFN-gamma alone. These data suggest that MV enhances NO production in CD46-expressing mouse macrophages through action of IFN-alpha /beta . Mouse macrophages expressing a human CD46 mutant lacking the cytoplasmic domains were highly susceptible to MV. These cells produced much lower levels of NO and IFN-alpha /beta upon infection by MV, suggesting the CD46 cytoplasmic domains enhanced IFN-alpha /beta production. When mouse macrophages expressing tailless human CD46 were exposed to culture medium from MV-infected mouse macrophages expressing intact human CD46, viral protein synthesis and development of cytopathic effects were suppressed. Pretreating the added culture medium with antibodies against IFN-alpha /beta abrogated these antiviral effects. Taken together, these findings suggest that expression of human CD46 in mouse macrophages enhances production of IFN-alpha /beta in response to MV infection, and IFN-alpha /beta synergizes with IFN-gamma to enhance NO production and restrict viral protein synthesis and virus replication. This novel function of human CD46 in mouse macrophages requires the CD46 cytoplasmic domains.

* Corresponding author. Mailing address: Department of Microbiology, University of Washington School of Medicine, Seattle, WA 98195. Phone: (206) 685-2162. Fax: (206) 543-8297. E-mail: timwong{at}u.washington.edu.

dagger Present address: National Kinki-chuo Hospital, Osaka, Japan.

Journal of Virology, February 2000, p. 1252-1257, Vol. 74, No. 3
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. Mol. Cell. Biol. Microbiol. Mol. Biol. Rev.
Clin. Vaccine Immunol. ALL ASM JOURNALS

Copyright © 2000 by the American Society for Microbiology. All rights reserved.