The attenuation phenotype conferred by the M gene of the influenza A/Ann Arbor/6/60 cold-adapted virus (H2N2) on the A/Korea/82 (H3N2) reassortant virus results from a gene constellation effect
Identifieur interne : 000C84 ( Istex/Checkpoint ); précédent : 000C83; suivant : 000C85The attenuation phenotype conferred by the M gene of the influenza A/Ann Arbor/6/60 cold-adapted virus (H2N2) on the A/Korea/82 (H3N2) reassortant virus results from a gene constellation effect
Auteurs : E. Kanta Subbarao [États-Unis] ; Mark Perkins [États-Unis] ; John J. Treanor [États-Unis] ; Brian R. Murphy [États-Unis]Source :
- Virus Research [ 0168-1702 ] ; 1992.
English descriptors
- Teeft :
- Amino acid, Attenuated, Attenuation, Attenuation phenotype, Betts, Constellation, Donor virus, Gene, Gene constellation, Gene constellation effect, Gene segment, Genetic stability, Hamster, Influenza, Influenza virus, Influenza virus vaccine, Lowest level, Maassab, Mdck cells, Mutation, Nasal turbinates, Nucleotide sequence, Phenotype, Polymerase, Polymerase genes, Present study, Reassortant, Reassortant virus, Reassortant viruses, Replication, Respiratory tract, Sequencing, Snyder, Standard error, Tcid, Turbinate, Vaccine, Viral, Virus, Virus genes, Virus vaccine, Virus vaccines, Wild type virus.
Abstract
Abstract: A single gene reassortant (SGR) virus that derived its M gene from the attenuated influenza A/Ann Arbor/6/60 cold-adapted (CA) donor virus and the remaining genes from the A/Korea/82 (H3N2) wild type (WT) virus (designated A/Korea/82 CA M-SGR) was previously shown to be attenuated in mice, hamsters, ferrets, and humans. The attenuation (ATT) phenotype of this SGR virus could result directly from an altered function of the mutant M gene product of the A/Ann Arbor/6/60 CA virus, which differs from the M gene of the A/Ann Arbor/6/60 WT virus at only one amino acid or, indirectly from a gene constellation effect in which ATT results from an inefficient interaction between the products of the M gene of the A/Ann Arbor/6/60 virus and other genes of the A/Korea/82 virus. Several lines of evidence from the present study are consistent with our interpretation that the ATT phenotype of the A/Korea/82 CA M-SGR results from a gene constellation effect. First, the A/Korea/82 CA M-SGR and an A/Korea/82 SGR containing the A/Ann Arbor/6/60 WT M gene were each restricted in replication in the upper and lower respiratory tract of mice compared with the A/Korea/82 WT virus. Second, an A/Udorn/72 CA M-SGR containing the M gene from the A/Ann Arbor/6/60 CA donor virus in a background of other genes derived from the A/Udorn/72 (H3N2) WT virus was not attenuated in the respiratory tract of mice. These data suggest that the change in the amino acid sequence of the M gene product from the A/Ann Arbor/6/60 WT to CA virus is not responsible for the ATT phenotype of the A/Korea/82 CA M-SGR. In addition, evidence of the genetic instability of the A/Korea/82 CA M-SGR is presented, specifically, an extragenic mutation that results in loss of the ATT phenotype. The implications of these findings for the ATT phenotype of the live attenuated reassortant viruses derived from the A/Ann Arbor/6/60 CA donor virus are discussed.
Url:
DOI: 10.1016/0168-1702(92)90098-T
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Kanta" last="Subbarao">E. Kanta Subbarao</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation></affiliation></author><author><name sortKey="Perkins, Mark" sort="Perkins, Mark" uniqKey="Perkins M" first="Mark" last="Perkins">Mark Perkins</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Treanor, John J" sort="Treanor, John J" uniqKey="Treanor J" first="John J." last="Treanor">John J. Treanor</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>University of Rochester School of Medicine, Division of Infectious Diseases, Rochester, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Murphy, Brian R" sort="Murphy, Brian R" uniqKey="Murphy B" first="Brian R." last="Murphy">Brian R. Murphy</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Virus Research</title><title level="j" type="abbrev">VIRUS</title><idno type="ISSN">0168-1702</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1992">1992</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="37">37</biblScope><biblScope unit="page" to="50">50</biblScope></imprint><idno type="ISSN">0168-1702</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0168-1702</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Amino acid</term><term>Attenuated</term><term>Attenuation</term><term>Attenuation phenotype</term><term>Betts</term><term>Constellation</term><term>Donor virus</term><term>Gene</term><term>Gene constellation</term><term>Gene constellation effect</term><term>Gene segment</term><term>Genetic stability</term><term>Hamster</term><term>Influenza</term><term>Influenza virus</term><term>Influenza virus vaccine</term><term>Lowest level</term><term>Maassab</term><term>Mdck cells</term><term>Mutation</term><term>Nasal turbinates</term><term>Nucleotide sequence</term><term>Phenotype</term><term>Polymerase</term><term>Polymerase genes</term><term>Present study</term><term>Reassortant</term><term>Reassortant virus</term><term>Reassortant viruses</term><term>Replication</term><term>Respiratory tract</term><term>Sequencing</term><term>Snyder</term><term>Standard error</term><term>Tcid</term><term>Turbinate</term><term>Vaccine</term><term>Viral</term><term>Virus</term><term>Virus genes</term><term>Virus vaccine</term><term>Virus vaccines</term><term>Wild type virus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: A single gene reassortant (SGR) virus that derived its M gene from the attenuated influenza A/Ann Arbor/6/60 cold-adapted (CA) donor virus and the remaining genes from the A/Korea/82 (H3N2) wild type (WT) virus (designated A/Korea/82 CA M-SGR) was previously shown to be attenuated in mice, hamsters, ferrets, and humans. The attenuation (ATT) phenotype of this SGR virus could result directly from an altered function of the mutant M gene product of the A/Ann Arbor/6/60 CA virus, which differs from the M gene of the A/Ann Arbor/6/60 WT virus at only one amino acid or, indirectly from a gene constellation effect in which ATT results from an inefficient interaction between the products of the M gene of the A/Ann Arbor/6/60 virus and other genes of the A/Korea/82 virus. Several lines of evidence from the present study are consistent with our interpretation that the ATT phenotype of the A/Korea/82 CA M-SGR results from a gene constellation effect. First, the A/Korea/82 CA M-SGR and an A/Korea/82 SGR containing the A/Ann Arbor/6/60 WT M gene were each restricted in replication in the upper and lower respiratory tract of mice compared with the A/Korea/82 WT virus. Second, an A/Udorn/72 CA M-SGR containing the M gene from the A/Ann Arbor/6/60 CA donor virus in a background of other genes derived from the A/Udorn/72 (H3N2) WT virus was not attenuated in the respiratory tract of mice. These data suggest that the change in the amino acid sequence of the M gene product from the A/Ann Arbor/6/60 WT to CA virus is not responsible for the ATT phenotype of the A/Korea/82 CA M-SGR. In addition, evidence of the genetic instability of the A/Korea/82 CA M-SGR is presented, specifically, an extragenic mutation that results in loss of the ATT phenotype. The implications of these findings for the ATT phenotype of the live attenuated reassortant viruses derived from the A/Ann Arbor/6/60 CA donor virus are discussed.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Subbarao, E Kanta" sort="Subbarao, E Kanta" uniqKey="Subbarao E" first="E. Kanta" last="Subbarao">E. Kanta Subbarao</name></region><name sortKey="Murphy, Brian R" sort="Murphy, Brian R" uniqKey="Murphy B" first="Brian R." last="Murphy">Brian R. Murphy</name><name sortKey="Perkins, Mark" sort="Perkins, Mark" uniqKey="Perkins M" first="Mark" last="Perkins">Mark Perkins</name><name sortKey="Treanor, John J" sort="Treanor, John J" uniqKey="Treanor J" first="John J." last="Treanor">John J. Treanor</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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