Biologic Potential of Amantadine-Resistant Influenza A Virus in an Avian Model
Identifieur interne : 002165 ( Main/Exploration ); précédent : 002164; suivant : 002166Biologic Potential of Amantadine-Resistant Influenza A Virus in an Avian Model
Auteurs : William J. Bean [États-Unis] ; Stephen C. Threlkeld [États-Unis] ; R. G. Webster [États-Unis]Source :
- Journal of Infectious Diseases [ 0022-1899 ] ; 1989.
Abstract
Amantadine has been accepted for both the treatment and prophylaxis of influenza A virus infections. Although amantadine-resistant mutants have been shown to be readily generated both in the laboratory and in children treated with rimantadine, little is known about their biologic properties, such as genetic stability, transmissibility, or pathogenicity, compared with the parental virus. This study examined these properties using an avian influenza virus, A/chicken/Pennsylvania/1370/83 (H5N2). Variants that were amantadine-resistant, virulent, and capable of competing with wild-type virus for transmission to susceptible hosts in the absence of the drug were selected. These amantadine-resistant variants were also genetically stable, showing no reversion to wild-type after six passages in birds over a period of >20 d. Thus, these virus variants had no detectable biologic impairment. The mutations conferring drug resistance were in the M2 polypeptide and were identical to mutations previously described in human amantadine-resistant virus. These results suggest that resistant mutants may have the potential to threaten the effective use of amantadine and rimantadine for the control of epidemic influenza.
Url:
DOI: 10.1093/infdis/159.6.1050
Affiliations:
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Webster</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:AB248E4F3082CAA749321D42776F68682DEE6BE8</idno><date when="1989" year="1989">1989</date><idno type="doi">10.1093/infdis/159.6.1050</idno><idno type="url">https://api.istex.fr/ark:/67375/HXZ-295TK68M-Q/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001551</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001551</idno><idno type="wicri:Area/Istex/Curation">001551</idno><idno type="wicri:Area/Istex/Checkpoint">000E86</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000E86</idno><idno type="wicri:doubleKey">0022-1899:1989:Bean W:biologic:potential:of</idno><idno type="wicri:Area/Main/Merge">002269</idno><idno type="wicri:Area/Main/Curation">002165</idno><idno type="wicri:Area/Main/Exploration">002165</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Biologic Potential of Amantadine-Resistant Influenza A Virus in an Avian Model</title><author><name sortKey="Bean, William J" sort="Bean, William J" uniqKey="Bean W" first="William J." last="Bean">William J. Bean</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis</wicri:cityArea></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Please address requests for reprints to Dr. William Bean, Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, P.O. Box 318, Memphis</wicri:cityArea></affiliation></author><author><name sortKey="Threlkeld, Stephen C" sort="Threlkeld, Stephen C" uniqKey="Threlkeld S" first="Stephen C." last="Threlkeld">Stephen C. Threlkeld</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis</wicri:cityArea></affiliation><affiliation></affiliation></author><author><name sortKey="Webster, R G" sort="Webster, R G" uniqKey="Webster R" first="R. G." last="Webster">R. G. Webster</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Tennessee</region></placeName><wicri:cityArea>Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Infectious Diseases</title><title level="j" type="abbrev">J Infect Dis.</title><idno type="ISSN">0022-1899</idno><idno type="eISSN">1537-6613</idno><imprint><publisher>The University of Chicago Press</publisher><date when="1989-06">1989</date><biblScope unit="vol">159</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1050">1050</biblScope><biblScope unit="page" to="1056">1056</biblScope></imprint><idno type="ISSN">0022-1899</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-1899</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Amantadine has been accepted for both the treatment and prophylaxis of influenza A virus infections. Although amantadine-resistant mutants have been shown to be readily generated both in the laboratory and in children treated with rimantadine, little is known about their biologic properties, such as genetic stability, transmissibility, or pathogenicity, compared with the parental virus. This study examined these properties using an avian influenza virus, A/chicken/Pennsylvania/1370/83 (H5N2). Variants that were amantadine-resistant, virulent, and capable of competing with wild-type virus for transmission to susceptible hosts in the absence of the drug were selected. These amantadine-resistant variants were also genetically stable, showing no reversion to wild-type after six passages in birds over a period of >20 d. Thus, these virus variants had no detectable biologic impairment. The mutations conferring drug resistance were in the M2 polypeptide and were identical to mutations previously described in human amantadine-resistant virus. These results suggest that resistant mutants may have the potential to threaten the effective use of amantadine and rimantadine for the control of epidemic influenza.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Tennessee</li></region></list><tree><country name="États-Unis"><region name="Tennessee"><name sortKey="Bean, William J" sort="Bean, William J" uniqKey="Bean W" first="William J." last="Bean">William J. Bean</name></region><name sortKey="Bean, William J" sort="Bean, William J" uniqKey="Bean W" first="William J." last="Bean">William J. Bean</name><name sortKey="Threlkeld, Stephen C" sort="Threlkeld, Stephen C" uniqKey="Threlkeld S" first="Stephen C." last="Threlkeld">Stephen C. Threlkeld</name><name sortKey="Webster, R G" sort="Webster, R G" uniqKey="Webster R" first="R. G." last="Webster">R. G. Webster</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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