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Journal of Virology, June 2008, p. 5606-5617, Vol. 82, No. 11
0022-538X/08/$08.00+0     doi:10.1128/JVI.02442-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Anticapsid Immunity Level, Not Viral Persistence Level, Correlates with the Progression of Theiler's Virus-Induced Demyelinating Disease in Viral P1-Transgenic Mice{triangledown}

Jinjong Myoung,1,{dagger} Young Yil Bahk,1,{ddagger} Hyun Seok Kang,1 Mauro C. Dal Canto,2 and Byung S. Kim1,2*

Department of Microbiology-Immunology,1 Department of Pathology, Northwestern University Medical School, Chicago, Illinois 606112

Received 13 November 2007/ Accepted 4 March 2008

Intracranial infection of Theiler's murine encephalomyelitis virus (TMEV) induces demyelination and a neurological disease in susceptible SJL/J (SJL) mice that resembles multiple sclerosis. While the virus is cleared from the central nervous system (CNS) of resistant C57BL/6 (B6) mice, it persists in SJL mice. To investigate the role of viral persistence and its accompanying immune responses in the development of demyelinating disease, transgenic mice expressing the P1 region of the TMEV genome (P1-Tg) were employed. Interestingly, P1-Tg mice with the B6 background showed severe reductions in both CD4+ and CD8+ T-cell responses to capsid epitopes, while P1-Tg mice with the SJL background displayed transient reductions following viral infection. Reduced antiviral immune responses in P1-Tg mice led to >100- to 1,000-fold increases in viral persistence at 120 days postinfection in the CNS of mice with both backgrounds. Despite the increased CNS TMEV levels in these P1-Tg mice, B6 P1-Tg mice developed neither neuropathological symptoms nor demyelinating lesions, and SJL P1-Tg mice developed significantly less severe TMEV-induced demyelinating disease. These results strongly suggest that viral persistence alone is not sufficient to induce disease and that the level of T-cell immunity to viral capsid epitopes is critical for the development of demyelinating disease in SJL mice.

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

{triangledown} Published ahead of print on 19 March 2008.

{dagger} Present address: G. W. Hooper Research Foundation, University of California, San Francisco, San Francisco, CA 94143.

{ddagger} Present address: Yonsei University, Seoul, South Korea.

Journal of Virology, June 2008, p. 5606-5617, Vol. 82, No. 11
0022-538X/08/$08.00+0     doi:10.1128/JVI.02442-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Hou, W., Kang, H. S., Kim, B. S. (2009). Th17 cells enhance viral persistence and inhibit T cell cytotoxicity in a model of chronic virus infection. JEM 206: 313-328 [Abstract] [Full Text]  


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