A single amino acid change at position 101 of VP1 in Theiler's virus attenuates the virus-induced central nervous system disease and reduces demyelinating lesions.
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A single VP1 mutation attenuates Theiler's virus demyelination in mice; leaves open translation to human CNS viral diseases or attenuation strategies.
We constructed a Theiler's virus mutant designated DA3304, in which the amino acid at position 101 of VP1 was changed from a threonine to an alanine. Because of this single amino acid change, DA3304 could still produce a biphasic central nervous system disease similar to that produced by the wild-type DA virus. However, DA3304 was significantly attenuated in both the acute and the chronic phases and induced smaller demyelinating lesions than the wild-type DA virus. The data are most compatible with the attenuated phenotype in DA3304 being due to the change of binding efficiency between the virus and receptor resulting from the physical alteration at the mutation site.
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Wada et al. (1994) studied this question.
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