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Journal of Virology, August 2002, p. 8335-8346, Vol. 76, No. 16
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.16.8335-8346.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Critical Role for Protein Tyrosine Phosphatase SHP-1 in Controlling Infection of Central Nervous System Glia and Demyelination by Theiler's Murine Encephalomyelitis Virus

Paul T. Massa,* Stacie L. Ropka, Sucharita Saha, Karen L. Fecenko, and Kathryn L. Beuler

Department of Neurology and Department of Microbiology and Immunology, Upstate Medical University, State University of New York, Syracuse, New York 13210

Received 25 February 2002/ Accepted 17 May 2002

We previously characterized the expression and function of the protein tyrosine phosphatase SHP-1 in the glia of the central nervous system (CNS). In the present study, we describe the role of SHP-1 in virus infection of glia and virus-induced demyelination in the CNS. For in vivo studies, SHP-1-deficient mice and their normal littermates received an intracerebral inoculation of an attenuated strain of Theiler's murine encephalomyelitis virus (TMEV). At various times after infection, virus replication, TMEV antigen expression, and demyelination were monitored. It was found that the CNS of SHP-1-deficient mice uniquely displayed demyelination and contained substantially higher levels of virus than did that of normal littermate mice. Many infected astrocytes and oligodendrocytes were detected in both brains and spinal cords of SHP-1-deficient but not normal littermate mice, showing that the virus replicated and spread at a much higher rate in the glia of SHP-1-deficient animals. To ascertain whether the lack of SHP-1 in the glia was primarily responsible for these differences, glial samples from these mice were cultured in vitro and infected with TMEV. As in vivo, infected astrocytes and oligodendrocytes of SHP-1-deficient mice were much more numerous and produced more virus than did those of normal littermate mice. These findings indicate that SHP-1 is a critical factor in controlling virus replication in the CNS glia and virus-induced demyelination.

* Corresponding author. Mailing address: Department of Neurology and Department of Microbiology and Immunology, Upstate Medical University, State University of New York, 750 E. Adams St., Syracuse, NY 13210. Phone: (315) 464-7606. Fax: (315) 464-6402. E-mail: massap{at}upstate.edu.

Journal of Virology, August 2002, p. 8335-8346, Vol. 76, No. 16
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.16.8335-8346.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Christophi, G. P., Hudson, C. A., Panos, M., Gruber, R. C., Massa, P. T. (2009). Modulation of Macrophage Infiltration and Inflammatory Activity by the Phosphatase SHP-1 in Virus-Induced Demyelinating Disease. J. Virol. 83: 522-539 [Abstract] [Full Text]  


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