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 Staeheli, P.
Right arrow Articles by Hausmann, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Staeheli, P.
Right arrow Articles by Hausmann, J.

 Previous Article  |  Next Article 

Journal of Virology, September 2001, p. 8216-8223, Vol. 75, No. 17
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.17.8216-8223.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Alpha/Beta Interferon Promotes Transcription and Inhibits Replication of Borna Disease Virus in Persistently Infected Cells

Peter Staeheli,1,* Maria Sentandreu,1 Axel Pagenstecher,2 and Jürgen Hausmann1

Department of Virology1 and Department of Neuropathology,2 University of Freiburg, D-79104 Freiburg, Germany

Received 26 February 2001/Accepted 24 May 2001

Borna disease virus (BDV) is a noncytolytic RNA virus that can replicate in the central nervous system (CNS) of mice. This study shows that BDV multiplication was efficiently blocked in transgenic mice that express mouse alpha-1 interferon (IFN-alpha 1) in astrocytes. To investigate whether endogenous virus-induced IFN might similarly restrict BDV, we used IFNAR0/0 mice, which lack a functional alpha/beta IFN (IFN-alpha /beta ) receptor. As would be expected if virus-induced IFN were important to control BDV infection, we found that cultured embryo cells of IFNAR0/0 mice supported viral multiplication, whereas cells from wild-type mice did not. Unexpectedly, however, BDV spread through the CNSs of IFNAR0/0 and wild-type mice with similar kinetics, suggesting that activation of endogenous IFN-alpha /beta genes in BDV-infected brains was too weak or occurred too late to be effective. Surprisingly, Northern blot analysis showed that the levels of the most abundant viral mRNAs in the brains of persistently infected IFNAR0/0 mice were about 20-fold lower than those in wild-type mice. In contrast, genomic viral RNA was produced in about a 10-fold excess in the brains of IFNAR0/0 mice. Human IFN-alpha 2 similarly enhanced transcription and simultaneously repressed replication of the BDV genome in persistently infected Vero cells. Thus, in persistently infected neurons and cultured cells, IFN-alpha /beta appears to freeze the BDV polymerase in the transcriptional mode, resulting in enhanced viral mRNA synthesis and suppressing viral genome replication.

* Corresponding author. Mailing address: Department of Virology, University of Freiburg, Hermann-Herder-Str. 11, D-79008 Freiburg, Germany. Phone: 49-761-203-6579. Fax.: 49-761-203-6562. E-mail: staeheli{at}ukl.uni-freiburg.de.

Journal of Virology, September 2001, p. 8216-8223, Vol. 75, No. 17
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.17.8216-8223.2001
Copyright © 2001, 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 © 2001 by the American Society for Microbiology. All rights reserved.