The study identifies specific capsid sequences (VP2 puff and VP1 loop regions) in TMEV that are critical for viral persistence in the central nervous system.
Warrants caution against clinical extrapolation from this animal model; leaves open the role of these sequences in human CNS viral persistence.
The demyelinating process in Theiler's murine encephalomyelitis virus (TMEV) infection in mice requires virus persistence in the central nervous system. Using recombinant TMEV assembled between the virulent GDVII and less virulent BeAn virus cDNAs, we now provide additional evidence supporting the localization of a persistence determinant to the leader P1 (capsid) sequences. Further, recombinant viruses in which BeAn sequences progressively replaced those of GDVII within the capsid starting at the leader NH2 terminus suggest that a conformational determinant requiring homologous sequences in both the VP2 puff and VP1 loop regions, which are in close contact on the virion surface, might underlie persistence.
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Adami et al. (1998) studied this question.
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