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 Aubagnac, S.
Right arrow Articles by Bureau, J.-F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Aubagnac, S.
Right arrow Articles by Bureau, J.-F.

 Previous Article  |  Next Article 

Journal of Virology, October 1999, p. 7965-7971, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Viral Load and a Locus on Chromosome 11 Affect the Late Clinical Disease Caused by Theiler's Virus

Stéphanie Aubagnac, Michel Brahic,* and Jean-François Bureau

Unité des Virus Lents, CNRS URA 1930, Institut Pasteur, 75724 Paris Cedex 15, France

Received 22 April 1999/Accepted 30 June 1999

Theiler's virus causes a persistent infection and a demyelinating disease of mice which is a model for multiple sclerosis. Susceptibility to viral persistence maps to several loci, including the interferon gamma locus. Inactivating the gene coding for the interferon gamma receptor makes 129/Sv mice susceptible to persistent infection and clinical disease, whereas inactivating the interferon gamma gene makes C57BL/6 mice susceptible to persistent infection but not to clinical disease. This difference in phenotype is due to the difference in genetic background. Clinical disease depends on high viral load and Tmevd5, a locus on chromosome 11. These results have consequences for the identification of viruses which might be implicated in multiple sclerosis.


* Corresponding author. Mailing address: Unité des Virus Lents, CNRS URA 1930, Institut Pasteur, 28, rue du Dr. Roux, 75724 Paris Cedex 15, France. Phone: 33 (0)1 45 68 87 70. Fax: 33 (0)1 40 61 31 67. E-mail: mbrahic{at}pasteur.fr.


Journal of Virology, October 1999, p. 7965-7971, Vol. 73, No. 10
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:

  • Myoung, J., Bahk, Y. Y., Kang, H. S., Dal Canto, M. C., Kim, B. S. (2008). Anticapsid Immunity Level, Not Viral Persistence Level, Correlates with the Progression of Theiler's Virus-Induced Demyelinating Disease in Viral P1-Transgenic Mice. J. Virol. 82: 5606-5617 [Abstract] [Full Text]  
  • Butterfield, R. J., Roper, R. J., Rhein, D. M., Melvold, R. W., Haynes, L., Ma, R. Z., Doerge, R. W., Teuscher, C. (2003). Sex-Specific Quantitative Trait Loci Govern Susceptibility to Theiler's Murine Encephalomyelitis Virus-Induced Demyelination. Genetics 163: 1041-1046 [Abstract] [Full Text]  
  • Aubagnac, S., Brahic, M., Bureau, J.-F. (2002). Bone Marrow Chimeras Reveal Non-H-2 Hematopoietic Control of Susceptibility to Theiler's Virus Persistent Infection. J. Virol. 76: 5807-5812 [Abstract] [Full Text]  
  • Thach, D. C., Kleeberger, S. R., Tucker, P. C., Griffin, D. E. (2001). Genetic Control of Neuroadapted Sindbis Virus Replication in Female Mice Maps to Chromosome 2 and Associates with Paralysis and Mortality. J. Virol. 75: 8674-8680 [Abstract] [Full Text]  
  • Aubagnac, S., Brahic, M., Bureau, J.-F. (2001). Viral Load Increases in SJL/J Mice Persistently Infected by Theiler's Virus after Inactivation of the {beta}2m Gene. J. Virol. 75: 7723-7726 [Abstract] [Full Text]  
  • Azoulay-Cayla, A., Dethlefs, S., Pérarnau, B., Larsson-Sciard, E.-L., Lemonnier, F. A., Brahic, M., Bureau, J.-F. (2000). H-2Db-/- Mice Are Susceptible to Persistent Infection by Theiler's Virus. J. Virol. 74: 5470-5476 [Abstract] [Full Text]