Temperature-Sensitive Mutants of Influenza Virus. V. Evaluation in Man of an Additional ts Recombinant Virus with a 39 C Shutoff Temperature
Identifieur interne : 002C05 ( Main/Exploration ); précédent : 002C04; suivant : 002C06Temperature-Sensitive Mutants of Influenza Virus. V. Evaluation in Man of an Additional ts Recombinant Virus with a 39 C Shutoff Temperature
Auteurs : Brian R. Murphy [États-Unis] ; David S. Hodes [États-Unis] ; Sandra R. Nusinoff [États-Unis] ; Susan Spring-Stewart [États-Unis] ; Eveline L. Tierney [États-Unis] ; Robert M. Chanock [États-Unis]Source :
- Journal of Infectious Diseases [ 0022-1899 ] ; 1974.
Abstract
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.
Url:
DOI: 10.1093/infdis/130.2.144
Affiliations:
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Le document en format XML
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<front><div type="abstract">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.</div>
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