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Journal of Virology, February 2000, p. 1477-1485, Vol. 74, No. 3
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Sialylation of the Host Receptor May Modulate Entry of Demyelinating Persistent Theiler's Virus

Lan Zhou,1,2 Yu Luo,2 Yan Wu,1 Jun Tsao,1,2 and Ming Luo1,2,*

Department of Microbiology1 and Center for Macromolecular Crystallography,2 University of Alabama at Birmingham, Birmingham, Alabama 35294

Received 16 August 1999/Accepted 19 October 1999

Theiler's murine encephalomyelitis virus (TMEV) is a picornavirus of the Cardiovirus genus. Certain strains of TMEV may cause a chronic demyelinating disease, which is very similar to multiple sclerosis in humans, associated with a persistent viral infection in the mouse central nervous system (CNS). Other strains of TMEV only cause an acute infection without persistence in the CNS. It has been shown that sialic acid is a receptor moiety only for the persistent TMEV strains and not for the nonpersistent strains. We report the effect of sialylation on cell surface on entry and the complex structure of DA virus, a persistent TMEV, and the receptor moiety mimic, sialyllactose, refined to a resolution of 3.0 Å. The ligand binds to a pocket on the viral surface, composed mainly of the amino acid residues from capsid protein VP2 puff B, in the vicinity of the VP1 loop and VP3 C terminus. The interaction of the receptor moiety with the persistent DA strain provides new understanding for the demyelinating persistent infection in the mouse CNS by TMEV.

* Corresponding author. Mailing address: Department of Microbiology, Center for Macromolecular Crystallography, University of Alabama at Birmingham, 260 Basic Health Sciences Bldg., 1918 University Blvd., Box 79 THT, Birmingham, AL 35294-0005. Phone: (205) 934-4259. Fax: (205) 975-9578. E-mail: ming{at}cmc.uab.edu.

Journal of Virology, February 2000, p. 1477-1485, Vol. 74, No. 3
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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