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 Messerle, M.
Right arrow Articles by Koszinowski, U. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Messerle, M.
Right arrow Articles by Koszinowski, U. H.

 Previous Article  |  Next Article 

J Virol, February 1998, p. 1377-1382, Vol. 72, No. 2
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Virus Attenuation after Deletion of the Cytomegalovirus Fc Receptor Gene Is Not due to Antibody Control

Irena Crnkovic'-Mertens,1 Martin Messerle,1 Irena Milotic',2 Uwe Szepan,1 Natalija Kucic',2 Astrid Krmpotic',2 Stipan Jonjic',2 and Ulrich H. Koszinowski1,*

Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, University of Munich, D-80336 Munich, Germany,1 and Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, 51000 Rijeka, Croatia2

Received 28 July 1997/Accepted 27 October 1997

The murine cytomegalovirus (MCMV) fcr-1 gene codes for a glycoprotein located at the surface of infected cells which strongly binds the Fc fragment of murine immunoglobulin G. To determine the biological significance of the fcr-1 gene during viral infection, we constructed MCMV fcr-1 deletion mutants and revertants. The fcr-1 gene was disrupted by insertion of the Escherichia coli lacZ gene. In another mutant, the marker gene was also deleted, by recombinase cre. As expected for its hypothetical role in immunoevasion, the infection of mice with fcr-1 deletion mutants resulted in significantly restricted replication in comparison with wild-type MCMV and revertant virus. In mutant mice lacking antibodies, however, the fcr-1 deletion mutants also replicated poorly. This demonstrated that the cell surface-expressed viral glycoprotein with FcR activity strongly modulates the virus-host interaction but that this biological function is not caused by the immunoglobulin binding property.

* Corresponding author. Mailing address: Max von Pettenkofer-Institut, Pettenkoferstr. 9a, D-80336 Munich, Germany. Phone: 49 89 5160 5290. Fax: 49 89 5160 5292. E-mail: koszinowski{at}m3401.mpk.med.uni-muenchen.de




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 © 1998 by the American Society for Microbiology. All rights reserved.