A mouse model demonstrates that a specific mutation (uracil at position 472) attenuates poliovirus neurovirulence, providing a useful indicator for testing genetic stability of new attenuating mutations.
May aid poliovirus vaccine stability testing; leaves open translation beyond mouse models.
A mutation in the genome of poliovirus type 3 that is known to reduce neurovirulence in humans similarly reduces neurovirulence in mice when incorporated into a mouse-adapted-human poliovirus recombinant. Viral recombinants with a uracil at nucleotide position 472 in the 5'-noncoding regions of their genomes are unable to replicate in the mouse brain. Viral recombinants with a cytosine at this position are neurovirulent in mice. Neurovirulence of poliovirus in mice may therefore prove to be a useful indicator of the genetic stability of new attenuating mutations created by site-directed mutagenesis.
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Monica et al. (1987) studied this question.
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