Molecular correlates of influenza A H5N1 virus pathogenesis in mice
Identifieur interne : 001823 ( Main/Exploration ); précédent : 001822; suivant : 001824Molecular correlates of influenza A H5N1 virus pathogenesis in mice
Auteurs : K. Subbarao [États-Unis] ; X. Lu [États-Unis] ; T. M Tumpey [États-Unis] ; C. B Smith [États-Unis] ; M. W Shaw [États-Unis] ; J. M Katz [États-Unis]Source :
- International congress series [ 0531-5131 ] ; 2001.
English descriptors
- Teeft :
- Acid residues, Avian influenza, Avian influenza viruses, Determinant, Embryonated hens, Gene segments, General virulence, High pathogenicity, Hong kong, Host range, Human cases, Human influenza, Influenza, Influenza apoptosis, Influenza virus, Influenza virus virulence, Influenza viruses, International congress series, Mammalian model, Mammalian species, Molecular basis, Molecular correlates, Molecular determinants, Mouse model, Mouse pathogenicity, Mouse pathogenicity phenotype, Pathogenicity, Pathogenicity phenotype, Phenotype, Respiratory disease, Respiratory illness, Respiratory tract, Sequence analysis, Specific residues, Subbarao, Virol, Virulence, Virus, Virus pathogenesis.
Abstract
Abstract: Background: In 1997, highly pathogenic avian influenza A H5N1 viruses caused 18 human cases of respiratory illness and six deaths in Hong Kong. The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. Methods: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. Results: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. Conclusions: Alone or in combination, these specific residues are the likely determinants of virulence of human H5N1 influenza viruses in this mammalian model.
Url:
DOI: 10.1016/S0531-5131(01)00635-5
Affiliations:
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Subbarao</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation><affiliation></affiliation></author><author><name sortKey="Lu, X" sort="Lu, X" uniqKey="Lu X" first="X" last="Lu">X. Lu</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Tumpey, T M" sort="Tumpey, T M" uniqKey="Tumpey T" first="T. M" last="Tumpey">T. 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B Smith</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Shaw, M W" sort="Shaw, M W" uniqKey="Shaw M" first="M. W" last="Shaw">M. W Shaw</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author><author><name sortKey="Katz, J M" sort="Katz, J M" uniqKey="Katz J" first="J. M" last="Katz">J. M Katz</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Influenza Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop G-16, 1600 Clifton Road, Atlanta, GA 30333</wicri:regionArea><placeName><region type="state">Géorgie (États-Unis)</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">International congress series</title><title level="j" type="abbrev">ICS</title><idno type="ISSN">0531-5131</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">1219</biblScope><biblScope unit="supplement">C</biblScope><biblScope unit="page" from="595">595</biblScope><biblScope unit="page" to="600">600</biblScope></imprint><idno type="ISSN">0531-5131</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0531-5131</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acid residues</term><term>Avian influenza</term><term>Avian influenza viruses</term><term>Determinant</term><term>Embryonated hens</term><term>Gene segments</term><term>General virulence</term><term>High pathogenicity</term><term>Hong kong</term><term>Host range</term><term>Human cases</term><term>Human influenza</term><term>Influenza</term><term>Influenza apoptosis</term><term>Influenza virus</term><term>Influenza virus virulence</term><term>Influenza viruses</term><term>International congress series</term><term>Mammalian model</term><term>Mammalian species</term><term>Molecular basis</term><term>Molecular correlates</term><term>Molecular determinants</term><term>Mouse model</term><term>Mouse pathogenicity</term><term>Mouse pathogenicity phenotype</term><term>Pathogenicity</term><term>Pathogenicity phenotype</term><term>Phenotype</term><term>Respiratory disease</term><term>Respiratory illness</term><term>Respiratory tract</term><term>Sequence analysis</term><term>Specific residues</term><term>Subbarao</term><term>Virol</term><term>Virulence</term><term>Virus</term><term>Virus pathogenesis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Background: In 1997, highly pathogenic avian influenza A H5N1 viruses caused 18 human cases of respiratory illness and six deaths in Hong Kong. The genes of the H5N1 viruses isolated from humans were derived from avian influenza viruses, with no evidence of reassortment with human influenza viruses. The molecular determinants of human pathogenesis were not evident. Methods: The BALB/c mouse was used as a mammalian model to evaluate the biological and molecular basis of human H5N1 virus pathogenesis. Molecular correlates of H5N1 virus pathogenicity for mice were sought by analyzing the nucleotide sequence of human H5N1 viruses. Results: Based on high and low lethality for mice, the pathogenicity phenotype of 15 human H5N1 viruses was characterized; nine viruses displayed a high, five a low, and one an intermediate pathogenicity phenotype. H5N1 viruses with a high pathogenicity phenotype replicated in multiple solid organs and caused depletion of peripheral blood leukocytes. Sequence analysis determined that five specific amino acids in four proteins correlated with pathogenicity in mice. Conclusions: Alone or in combination, these specific residues are the likely determinants of virulence of human H5N1 influenza viruses in this mammalian model.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Géorgie (États-Unis)</li></region></list><tree><country name="États-Unis"><region name="Géorgie (États-Unis)"><name sortKey="Subbarao, K" sort="Subbarao, K" uniqKey="Subbarao K" first="K" last="Subbarao">K. Subbarao</name></region><name sortKey="Katz, J M" sort="Katz, J M" uniqKey="Katz J" first="J. M" last="Katz">J. M Katz</name><name sortKey="Lu, X" sort="Lu, X" uniqKey="Lu X" first="X" last="Lu">X. Lu</name><name sortKey="Shaw, M W" sort="Shaw, M W" uniqKey="Shaw M" first="M. W" last="Shaw">M. W Shaw</name><name sortKey="Smith, C B" sort="Smith, C B" uniqKey="Smith C" first="C. B" last="Smith">C. B Smith</name><name sortKey="Tumpey, T M" sort="Tumpey, T M" uniqKey="Tumpey T" first="T. M" last="Tumpey">T. 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