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J. Virol., 12 1995, 7601-7605, Vol 69, No. 12
Copyright © 1995, American Society for Microbiology

Role of mutations G-480 and C-6203 in the attenuation phenotype of Sabin type 1 poliovirus

A McGoldrick, AJ Macadam, G Dunn, A Rowe, J Burlison, PD Minor, J Meredith, DJ Evans and JW Almond
School of Animal and Microbial Sciences, University of Reading, Whiteknigts, Reading, United Kingdom.

Of the 55 point mutations which distinguish the type 1 poliovirus vaccine strain (Sabin 1) from its neurovirulent progenitor (P1/Mahoney), two have been strongly implicated by previous studies as determinants of the attenuation phenotype. A change of an A to a G at position 480, located within the 5' noncoding region, has been suggested to be the major attenuating mutation, analogous to the mutations at positions 481 and 472 in poliovirus types 2 and 3, respectively. In addition, the change of a U to a C at position 6203, resulting in an amino acid change in the polymerase protein 3D, has also been implicated as a determinant of attenuation, albeit to a lesser extent. To assess the contributions of these mutations to attenuation and temperature sensitivity, reciprocal changes were generated at these positions in infectious cDNA clones of Sabin 1 and P1/Mahoney. Assays in tissue culture and primates indicated that the two mutations make some contribution to the temperature sensitivity of the Sabin 1 strain but that neither is a strong determinant of attenuation.

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