Key result
Amino acid substitutions or deletion of the antigenic site 1 in a chimeric type 1/type 2 poliovirus yielded neutralization-escape mutants that were attenuated or devoid of neurovirulence in mice.
Mutations or deletions in the antigenic site 1 of a chimeric poliovirus attenuate its neurovirulence in mice.
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Attenuated escape mutants may inform poliovirus vaccine strategies; animal data leave open human translation.
A chimeric type 1/type 2 poliovirus (v510), in which the antigenic site 1 (Ag1) of poliovirus type 1 (PV-1) Mahoney was replaced by the corresponding site of poliovirus type 2 (PV-2) Lansing, is known to be neurovirulent for mice and neutralized by both type 1 and type 2 monoclonal antibodies. Neutralization-escape mutants to monoclonal antibodies specifically recognizing the PV-2 sequence were obtained from v510. The nucleotide sequence and the mouse neurovirulence of mutants were determined. Amino acid substitutions obtained inside the replaced sequence, at positions 95 and 99, and outside this site, at positions 93 or 104, rendered the virus attenuated for mice. One of the escape mutants harboured a deletion of the entire substituted nonapeptide sequence in v510. This particular virus, which is a PV-1 Mahoney lacking the natural Ag1 loop, does not react with PV-2-specific monoclonal antibodies, has a ts phenotype, is heat-labile and is devoid of neurovirulence for mice.
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Couderc et al. (1991) studied Poliovirus infection. Neutralization-escape mutants of chimeric type 1/type 2 poliovirus (v510) was evaluated on Mouse neurovirulence and viral phenotype. Amino acid substitutions or deletion of the antigenic site 1 in a chimeric type 1/type 2 poliovirus yielded neutralization-escape mutants that were attenuated or devoid of neurovirulence in mice.
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