J Gen Virol Try Microbiology Online
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Gen Virol 87 (2006), 2663-2667; DOI 10.1099/vir.0.82024-0

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary tables
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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 arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnson, N.
Right arrow Articles by Fooks, A. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnson, N.
Right arrow Articles by Fooks, A. R.
Agricola
Right arrow Articles by Johnson, N.
Right arrow Articles by Fooks, A. R.
© 2006 Society for General Microbiology

Short Communication

Lyssavirus infection activates interferon gene expression in the brain

Nicholas Johnson1, Clive S. McKimmie2, Karen L. Mansfield1, Philip R. Wakeley3, Sharon M. Brookes1, John K. Fazakerley2 and Anthony R. Fooks1

1 Rabies and Wildlife Zoonoses Group (WHO Collaborating Centre for the Characterization of Rabies and Rabies-related Viruses), Department of Virology, Veterinary Laboratories Agency (Weybridge), Addlestone, Surrey KT15 3NB, UK
2 Virology, Centre for Infectious Diseases, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH9 1QH, UK
3 Technology Transfer Unit, Veterinary Laboratories Agency (Weybridge), Addlestone, Surrey KT15 3NB, UK

Correspondence
Nicholas Johnson
n.johnson2{at}vla.defra.gsi.gov.uk

To investigate the innate immune response within the brain to lyssavirus infection, key transcripts indicative of innate defences were measured in a mouse model system. Following infection with Rabies virus, transcript levels for type 1 interferons (IFN-{alpha} and -beta), the inflammatory mediator interleukin 6 (IL-6) and the antiviral protein Mx1 increased in the brains of mice. Intracranial inoculation resulted in the early detection of virus replication and rapid expression within the brain of the innate immune response genes. Transcripts for type 1 IFNs declined as the disease progressed. Peripheral, extraneural inoculation delayed the host response until virus entered the brain, but then resulted in a large increase in the level of IFN-beta, IL-6 and Mx1 transcripts. Induction of this response was also observed following infection with the related European bat lyssaviruses, a group of zoonotic viruses capable of causing fatal, rabies-like disease in mammalian species.

Supplementary tables showing primer sequences and lyssavirus isolates used are available in JGV Online.




This article has been cited by other articles:


Home page
J. Gen. Virol.Home page
N. Johnson, A. Vos, L. Neubert, C. Freuling, K. L. Mansfield, I. Kaipf, A. Denzinger, D. Hicks, A. Nunez, R. Franka, et al.
Experimental study of European bat lyssavirus type-2 infection in Daubenton's bats (Myotis daubentonii)
J. Gen. Virol., November 1, 2008; 89(11): 2662 - 2672.
[Abstract] [Full Text] [PDF]


Home page
J. Gen. Virol.Home page
R. Fragkoudis, L. Breakwell, C. McKimmie, A. Boyd, G. Barry, A. Kohl, A. Merits, and J. K. Fazakerley
The type I interferon system protects mice from Semliki Forest virus by preventing widespread virus dissemination in extraneural tissues, but does not mediate the restricted replication of avirulent virus in central nervous system neurons
J. Gen. Virol., December 1, 2007; 88(12): 3373 - 3384.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
INT J SYST EVOL MICROBIOL MICROBIOLOGY J GEN VIROL
J MED MICROBIOL ALL SGM JOURNALS
Copyright © 2006 by the Society for General Microbiology.