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Two recombinant temperature-sensitive (ts) influenza A/Hong Kong/68 (H3N2) viruses that exhibited a marked decrease in efficiency of plaque formation at 39 C but that had lesions in different cistrons of the influenza A virus genome were evaluated for level of virulence in man. Both viruses retained the capacity to cause mild influenzal illness that was less severe than that caused by wild-type virus but more severe than that of the candidate influenza A/HK/68-ts-1[E] vaccine virus. These studies indicated that two viruses with similar temperature sensitivity but different genetic lesions had a similar level of attenuation for man. This observation supports the suggestion that it is the degree of defectiveness, i.e., temperature sensitivity, of a mutant virus and not the loss of a specific biochemical function that is the determinant of attenuation of these viruses for man.
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Murphy et al. (1974) studied this question.
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