Temperature-Sensitive Mutants of Influenza A Virus. XIV. Production and Evaluation of Influenza A/Georgia/74-ts-I[E] Recombinant Viruses in Human Adults
Identifieur interne : 002A50 ( Main/Exploration ); précédent : 002A49; suivant : 002A51Temperature-Sensitive Mutants of Influenza A Virus. XIV. Production and Evaluation of Influenza A/Georgia/74-ts-I[E] Recombinant Viruses in Human Adults
Auteurs : Douglas D. Richman [États-Unis] ; Brian R. Murphy [États-Unis] ; Robert B. Belshe [États-Unis] ; Harold M. Rusten [États-Unis] ; Robert M. Chanock [États-Unis] ; Neil R. Blacklow [États-Unis] ; Thomas A. Parrino [États-Unis] ; Frederick B. Rose [États-Unis] ; Myron M. Levine [États-Unis] ; Ellis Caplan [États-Unis]Source :
- Journal of Infectious Diseases [ 0022-1899 ] ; 1977.
Abstract
The two temperature-sensltlve (ts) lesions present in influenza A/Hong Kong/68-ts- 1[E] (H3N268) virus were transferred via genetic reassortment to influenza A/Georgia/74 (H3N274) wild-type virus. A recombinant clone possessing both ts lesions and the shutoff temperature of 38 C of the Hong Kong/68 ts donor and the two surface antigens of the Georgia/74 wild-type virus was administered to 32 seronegative adult volunteers. Thirty-one volunteers were infected, of whom only five experienced mild afebrile upper respiratory tract illness. The wild-type recipient virus was a cloned population that induced illness in five of six infected volunteers. Therefore, the attenuation exhibited by the Georgia/74-ts-l[E] virus could reasonably be assumed to be due to the acquisition of the two ts-1[E] lesions by the Georgia/74 wild-type virus. The serum and nasal wash antibody responses of the ts-l [E] vaccinees were equivalent to those of the volunteers who received wild-type virus. The two ts lesions present in the Hong Kong/68-ts-1[E] virus have now been transferred three times to a wild-type virus bearing a new hemagglutinin, and in each instance the new ts recombinant exhibited a similar, satisfactory level of attenuation and antigenicity for adults. It seems likely that the transfer of the ts-1[E] lesions to any new influenza virus will regularly result in attenuation of a recombinant virus possessing the new surface antigens.
Url:
DOI: 10.1093/infdis/136.2.256
Affiliations:
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<wicri:cityArea>From the Division of Adult Infectious Diseases, University Hospital, Boston, Massachusetts, Baltimore, Bethesda</wicri:cityArea>
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<author><name sortKey="Belshe, Robert B" sort="Belshe, Robert B" uniqKey="Belshe R" first="Robert B." last="Belshe">Robert B. Belshe</name>
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<author><name sortKey="Rusten, Harold M" sort="Rusten, Harold M" uniqKey="Rusten H" first="Harold M." last="Rusten">Harold M. Rusten</name>
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<placeName><region type="state">Maryland</region>
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<wicri:cityArea>From the Division of Adult Infectious Diseases, University Hospital, Boston, Massachusetts, Baltimore, Bethesda</wicri:cityArea>
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<author><name sortKey="Chanock, Robert M" sort="Chanock, Robert M" uniqKey="Chanock R" first="Robert M." last="Chanock">Robert M. Chanock</name>
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<placeName><region type="state">Maryland</region>
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<wicri:cityArea>From the Division of Adult Infectious Diseases, University Hospital, Boston, Massachusetts, Baltimore, Bethesda</wicri:cityArea>
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<author><name sortKey="Blacklow, Neil R" sort="Blacklow, Neil R" uniqKey="Blacklow N" first="Neil R." last="Blacklow">Neil R. Blacklow</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Maryland</region>
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<wicri:cityArea>From the Division of Adult Infectious Diseases, University Hospital, Boston, Massachusetts, Baltimore, Bethesda</wicri:cityArea>
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<author><name sortKey="Parrino, Thomas A" sort="Parrino, Thomas A" uniqKey="Parrino T" first="Thomas A." last="Parrino">Thomas A. Parrino</name>
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<placeName><region type="state">Maryland</region>
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<wicri:cityArea>From the Division of Adult Infectious Diseases, University Hospital, Boston, Massachusetts, Baltimore, Bethesda</wicri:cityArea>
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<wicri:cityArea>From the Division of Adult Infectious Diseases, University Hospital, Boston, Massachusetts, Baltimore, Bethesda</wicri:cityArea>
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<front><div type="abstract">The two temperature-sensltlve (ts) lesions present in influenza A/Hong Kong/68-ts- 1[E] (H3N268) virus were transferred via genetic reassortment to influenza A/Georgia/74 (H3N274) wild-type virus. A recombinant clone possessing both ts lesions and the shutoff temperature of 38 C of the Hong Kong/68 ts donor and the two surface antigens of the Georgia/74 wild-type virus was administered to 32 seronegative adult volunteers. Thirty-one volunteers were infected, of whom only five experienced mild afebrile upper respiratory tract illness. The wild-type recipient virus was a cloned population that induced illness in five of six infected volunteers. Therefore, the attenuation exhibited by the Georgia/74-ts-l[E] virus could reasonably be assumed to be due to the acquisition of the two ts-1[E] lesions by the Georgia/74 wild-type virus. The serum and nasal wash antibody responses of the ts-l [E] vaccinees were equivalent to those of the volunteers who received wild-type virus. The two ts lesions present in the Hong Kong/68-ts-1[E] virus have now been transferred three times to a wild-type virus bearing a new hemagglutinin, and in each instance the new ts recombinant exhibited a similar, satisfactory level of attenuation and antigenicity for adults. It seems likely that the transfer of the ts-1[E] lesions to any new influenza virus will regularly result in attenuation of a recombinant virus possessing the new surface antigens.</div>
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<tree><country name="États-Unis"><region name="Maryland"><name sortKey="Richman, Douglas D" sort="Richman, Douglas D" uniqKey="Richman D" first="Douglas D." last="Richman">Douglas D. Richman</name>
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<name sortKey="Belshe, Robert B" sort="Belshe, Robert B" uniqKey="Belshe R" first="Robert B." last="Belshe">Robert B. Belshe</name>
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<name sortKey="Murphy, Brian R" sort="Murphy, Brian R" uniqKey="Murphy B" first="Brian R." last="Murphy">Brian R. Murphy</name>
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