Abstract
Attenuated poliovirus strains induce less interferon-α(IFN-α) in human leukocyte cultures than their parental wild-type strains or other neurovirulent strains. We have used a set of type 3 Leon/Sabin recombinant poliovirus strains to show that production of IFN in this system is closely associated with the genomic region that codes for capsid protein VP3; a mutation in this gene also causes the temperature sensitivity of the attenuated Sabin 3 strain and is partly responsible for the loss of neurovirulence of this vaccine strain. Sixteen independent poliovirus isolates, derived from the Sabin 3 virus but showing in vitro and in vivo markers of neurovirulence, were also tested. These gave IFN yields equivalent to or higher than those obtained with the neurovirulent Leon type 3 poliovirus. The relatively low IFN yields with the Sabin 3 virus seem not to be a direct consequence of its temperature sensitivity, but the two properties coincide with all the type 3 poliovirus strains tested.
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