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J Virol, February 1998, p. 1020-1027, Vol. 72, No. 2
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

A Spontaneous Low-Pathogenic Variant of Theiler's Virus Contains an Amino Acid Substitution within the Predominant VP1233-250 T-Cell Epitope

Byung S. Kim,* Robert L. Yauch,dagger Young Yil Bahk, Jeong-Ah Kang, Mauro C. Dal Canto, and Catherine Kappel HallDagger

Departments of Microbiology-Immunology and Pathology and Institute for Neuroscience, Northwestern University Medical School, Chicago, Illinois 60611

Received 2 July 1997/Accepted 30 October 1997

Theiler's murine encephalomyelitis virus (TMEV) induces immune-mediated demyelination after intracerebral inoculation of the virus into susceptible mouse strains. We isolated from a TMEV BeAn 8386 viral stock, a low-pathogenic variant which requires greater than a 10,000-fold increase in viral inoculation for the manifestation of detectable clinical signs. Intracerebral inoculation of this variant virus induced a strong, long-lasting, protective immunity from the demyelinating disease caused by pathogenic TMEV. The levels of antibodies to the whole virus as well as to the major linear epitopes were similar in mice infected with either the variant or wild-type virus. However, persistence of the variant virus in the central nervous system (CNS) of mice was significantly lower than that of the pathogenic virus. In addition, the T-cell response to the predominant VP1 (VP1233-250) epitope in mice infected with the variant virus was significantly weaker than that in mice infected with the parent virus, while similar T-cell responses were induced against another predominant epitope (VP274-86). Further analyses indicated that a change of lysine to arginine at position 244 of VP1, which is the only amino acid difference in the P1 region, is responsible for such differential T-cell recognition. Thus, the difference in the T-cell reactivity to this VP1 region as well as the low level of viral persistence in the CNS may account for the low pathogenicity of this spontaneous variant virus.

* Corresponding author. Mailing address: Department of Microbiology-Immunology, Northwestern University Medical School, 303 E. Chicago Ave., Chicago, IL 60611. Phone: (312) 503-8693. Fax: (312) 503-1339. E-mail: bskim{at}nwu.edu.

dagger Present address: Dana-Farber Cancer Research Institute, Harvard Medical School, Boston, MA 02115.

Dagger Present address: Science Applications International Corp., Frederick, MD 21702.




This article has been cited by other articles:

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  • 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]  
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  • Inoue, A., Koh, C.-S., Yamazaki, M., Yagita, H. (1999). Effect of Anti-B7-1 and Anti-B7-2 mAb on Theiler's Murine Encephalomyelitis Virus-Induced Demyelinating Disease. J. Immunol. 163: 6180-6186 [Abstract] [Full Text]  
  • Kim, B. S., Bahk, Y. Y., Kang, H.-K., Yauch, R. L., Kang, J.-A., Park, M.-J., Ponzio, N. M. (1999). Diverse Fine Specificity and Receptor Repertoire of T Cells Reactive to the Major VP1 Epitope (VP1230-250) of Theiler's Virus: V{beta} Restriction Correlates with T Cell Recognition of the C-Terminal Residue. J. Immunol. 162: 7049-7057 [Abstract] [Full Text]  
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