The temperature sensitivity of the Sabin type 1 poliovirus is likely due to the initiation step of RNA chain synthesis rather than RNA polymerization elongation activity.
Supports initiation over elongation for Sabin ts mechanism; hypothesis-generating for attenuation, no practice change.
Determinants of attenuation in the Sabin type 1 strain of poliovirus are located in the 5' noncoding region, the capsid coding region and the viral RNA-dependent RNA polymerase (3Dpol) coding region. These mutations also contribute to a temperature sensitive pheno-type of virus replication. We have cloned and expressed the Sabin 1 virus 3Dpol) protein which contains three amino acid differences from the wild-type (Mahoney) sequence, as well as a wild- type polymerase containing only a single Sabin amino acid substitution at nt 6203. These enzymes have been examined and compared for temperature sensitive polymerase activity. Wild-type and mutated polymerases demonstrated identical specific activities at 30, 35 and 39 degrees C. All three showed the same kinetics of heat inactivation after pre-incubation at elevated temperatures. Thus the contribution of Sabin 3Dpol sequences to the inability of the virus to grow at elevated temperatures must lie in a function or activity of the enzyme other than RNA polymerization. A likely reaction is the initiation step of RNA chain synthesis.
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Baker et al. (1995) studied this question.
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