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Journal of Virology, August 2001, p. 7494-7505, Vol. 75, No. 16
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.16.7494-7505.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Prolonged Gray Matter Disease without Demyelination Caused by Theiler's Murine Encephalomyelitis Virus with a Mutation in VP2 Puff B

Ikuo Tsunoda,1 Yoshiaki Wada,1,dagger Jane E. Libbey,1 Thomas S. Cannon,1 Frank G. Whitby,2 and Robert S. Fujinami1,*

Department of Neurology, University of Utah School of Medicine,1 and Department of Biochemistry, University of Utah,2 Salt Lake City, Utah 84132

Received 5 February 2001/Accepted 2 May 2001

Theiler's murine encephalomyelitis virus (TMEV) is divided into two subgroups based on neurovirulence. During the acute phase, DA virus infects cells in the gray matter of the central nervous system (CNS). Throughout the chronic phase, DA virus infects glial cells in the white matter, causing demyelinating disease. Although GDVII virus also infects neurons in the gray matter, infected mice developed a severe polioencephalomyelitis, and no virus is detected in the white matter or other areas in the CNS in rare survivors. Several sequence differences between the two viruses are located in VP2 puff B and VP1 loop II, which are located near each other, close to the proposed receptor binding site. We constructed a DA virus mutant, DApBL2M, which has the VP1 loop II of GDVII virus and a mutation at position 171 in VP2 puff B. While DApBL2M virus replicated less efficiently than DA virus during the acute phase, DApBL2M-induced acute polioencephalitis was comparable to that in DA virus infection. Interestingly, during the chronic phase, DApBL2M caused prolonged gray matter disease in the brain without white matter involvement in the spinal cord. This is opposite what is observed during wild-type DA virus infection. Our study is the first to demonstrate that conformational differences via interaction of VP2 puff B and VP1 loop II between GDVII and DA viruses can play an important role in making the transition of infection from the gray matter in the brain to the spinal cord white matter during TMEV infection.

* Corresponding author. Mailing address: Department of Neurology, University of Utah School of Medicine, 30 North 1900 East, Room 3R330, Salt Lake City, UT 84132. Phone: (801) 585-3305. Fax: (801) 585-3311. E-mail: Robert.Fujinami{at}hsc.utah.edu.

dagger Present address: Department of Neurology, Nissan Tamagawa Hospital, 4-8-1 Seta, Setagaya-ku, Tokyo 158-0095, Japan.

Journal of Virology, August 2001, p. 7494-7505, Vol. 75, No. 16
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.16.7494-7505.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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