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Comparison of the complete nucleotide sequences of the genomes of the neurovirulent poliovirus P3/Leon/37 and its attenuated Sabin vaccine derivative P3/Leon 12a1b.

Proceedings of the National Academy of Sciences of the United States of America, 01 Mar 1984, 81(5):1539-1543
https://doi.org/10.1073/pnas.81.5.1539 PMID: 6324200 PMCID: PMC344872

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Abstract 

As part of a study into the molecular basis of attenuation and reversion to neurovirulence in the Sabin poliovirus vaccines, we have determined the complete nucleotide sequence of a cloned DNA copy of the genome of P3/Leon/37, the neurovirulent progenitor of the type 3 Sabin vaccine strain, P3/Leon 12a1b. Comparison of the sequence with that which we previously obtained for the vaccine strain [Stanway, G., Cann, A. J., Hauptmann, R., Hughes, P., Clarke, L. D., Mountford, R. C., Minor, P. D., Schild, G. C. & Almond, J. W. (1983) Nucleic Acids Res. 11, 5629-5643] indicates that attenuation has been brought about by a maximum of 10 point mutations, at least 5 of which are likely to be of minor significance. Predicted amino acid sequences of all the known virus-encoded proteins show that amino acid substitutions have occurred at only three positions. Two of these are in structural proteins (i.e., Ser----Phe in VP3 and Lys----Arg in VP1), and the third, Thr----Ala, is in the nonstructural protein P2-3b. The distribution and nature of nucleotide and amino acid sequence differences suggest that a single base substitution may be responsible for the attenuated phenotype of the vaccine strain.

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Proc Natl Acad Sci U S A. 1984 Mar; 81(5): 1539–1543.
PMCID: PMC344872
PMID: 6324200

Comparison of the complete nucleotide sequences of the genomes of the neurovirulent poliovirus P3/Leon/37 and its attenuated Sabin vaccine derivative P3/Leon 12a1b.

G Stanway, P J Hughes, R C Mountford, P Reeve, P D Minor, G C Schild, and J W Almond
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Abstract

As part of a study into the molecular basis of attenuation and reversion to neurovirulence in the Sabin poliovirus vaccines, we have determined the complete nucleotide sequence of a cloned DNA copy of the genome of P3/Leon/37, the neurovirulent progenitor of the type 3 Sabin vaccine strain, P3/Leon 12a1b. Comparison of the sequence with that which we previously obtained for the vaccine strain [Stanway, G., Cann, A. J., Hauptmann, R., Hughes, P., Clarke, L. D., Mountford, R. C., Minor, P. D., Schild, G. C. & Almond, J. W. (1983) Nucleic Acids Res. 11, 5629-5643] indicates that attenuation has been brought about by a maximum of 10 point mutations, at least 5 of which are likely to be of minor significance. Predicted amino acid sequences of all the known virus-encoded proteins show that amino acid substitutions have occurred at only three positions. Two of these are in structural proteins (i.e., Ser----Phe in VP3 and Lys----Arg in VP1), and the third, Thr----Ala, is in the nonstructural protein P2-3b. The distribution and nature of nucleotide and amino acid sequence differences suggest that a single base substitution may be responsible for the attenuated phenotype of the vaccine strain.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.
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