Influenza resistance to zanamivir generated in ferrets
Identifieur interne : 001829 ( Main/Exploration ); précédent : 001828; suivant : 001830Influenza resistance to zanamivir generated in ferrets
Auteurs : M. Louise Herlocher [États-Unis] ; Rob Fenton [Royaume-Uni] ; Andrew Merry [États-Unis] ; Stephanie Elias [États-Unis] ; Arnold S. Monto [États-Unis]Source :
- International congress series [ 0531-5131 ] ; 2001.
English descriptors
- Teeft :
- Agents chemother, Amantadine, Amino, Amino acids, Animal model, Antimicrob, Bethell, Clone, Days pretreat, Herlocher, Immunocompromised child, Influenza, Influenza clones, Influenza neuraminidase, Influenza resistance, Influenza virus, Influenza virus infection, Influenza viruses, Inhibitor, International congress series, Mdck, Mdck cells, Mutation, Nasal, Nasal wash, Nasal washes, Neuraminidase, Neuraminidase gene, Neuraminidase inhibitor, Parent virus, Pretreated, Resistant clones, Resistant virus, Tissue culture, Virology, Virus, Zanamivir.
Abstract
Abstract: Zanamivir (4-Guanidino-2,4-dideoxy-2,3-dehydro-N-acetylneuraminic acid), an anti-neuraminidase drug, is highly effective in the treatment of influenza. Influenza resistance to zanamivir has proved difficult to raise. Two neuraminidase mutations leading to resistance in vitro have been identified in several viruses—glu 119 gly and arg 292 lys. Only one resistant virus (an influenza B clone) has been observed in vivo in an immunocompromised child. This series of experiments sought to develop A/LA/1/87 (H3N2) influenza clones resistant to zanamivir in a ferret model. Using this model resistance to amantadine was easily developed within 6 days of treatment. Although most ferrets treated with zanamivir shed virus in the nasal wash, all ferrets were protected from fever and illness when treated with zanamivir. When ferrets were infected with nasal wash from ferrets previously infected with A/LA/1/87 (H3N2) and treated with zanamivir, 20 clones from their nasal wash grew on MDCK cells in the presence of 1 μM zanamivir. Sequencing of the NA genes of these clones revealed no mutations at positions 119 or 292. However, a nucleotide mutation at position 685 was observed in five of the clones. Sequencing of HA1 and HA2 for all genes is underway. Although characterization of the 20 clones is not complete, we can say that resistance to zanamivir will not arise as quickly or with the same frequency as does resistance to amantadine.
Url:
DOI: 10.1016/S0531-5131(01)00365-X
Affiliations:
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Monto</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Epidemiology, School of Public Health, University of Michigan, 109 Observatory Street, Ann Arbor, MI 48109-2029</wicri:regionArea><placeName><region type="state">Michigan</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="863">863</biblScope><biblScope unit="page" to="877">877</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>Agents chemother</term><term>Amantadine</term><term>Amino</term><term>Amino acids</term><term>Animal model</term><term>Antimicrob</term><term>Bethell</term><term>Clone</term><term>Days pretreat</term><term>Herlocher</term><term>Immunocompromised child</term><term>Influenza</term><term>Influenza clones</term><term>Influenza neuraminidase</term><term>Influenza resistance</term><term>Influenza virus</term><term>Influenza virus infection</term><term>Influenza viruses</term><term>Inhibitor</term><term>International congress series</term><term>Mdck</term><term>Mdck cells</term><term>Mutation</term><term>Nasal</term><term>Nasal wash</term><term>Nasal washes</term><term>Neuraminidase</term><term>Neuraminidase gene</term><term>Neuraminidase inhibitor</term><term>Parent virus</term><term>Pretreated</term><term>Resistant clones</term><term>Resistant virus</term><term>Tissue culture</term><term>Virology</term><term>Virus</term><term>Zanamivir</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Zanamivir (4-Guanidino-2,4-dideoxy-2,3-dehydro-N-acetylneuraminic acid), an anti-neuraminidase drug, is highly effective in the treatment of influenza. Influenza resistance to zanamivir has proved difficult to raise. Two neuraminidase mutations leading to resistance in vitro have been identified in several viruses—glu 119 gly and arg 292 lys. Only one resistant virus (an influenza B clone) has been observed in vivo in an immunocompromised child. This series of experiments sought to develop A/LA/1/87 (H3N2) influenza clones resistant to zanamivir in a ferret model. Using this model resistance to amantadine was easily developed within 6 days of treatment. Although most ferrets treated with zanamivir shed virus in the nasal wash, all ferrets were protected from fever and illness when treated with zanamivir. When ferrets were infected with nasal wash from ferrets previously infected with A/LA/1/87 (H3N2) and treated with zanamivir, 20 clones from their nasal wash grew on MDCK cells in the presence of 1 μM zanamivir. Sequencing of the NA genes of these clones revealed no mutations at positions 119 or 292. However, a nucleotide mutation at position 685 was observed in five of the clones. Sequencing of HA1 and HA2 for all genes is underway. Although characterization of the 20 clones is not complete, we can say that resistance to zanamivir will not arise as quickly or with the same frequency as does resistance to amantadine.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Michigan</li></region></list><tree><country name="États-Unis"><noRegion><name sortKey="Herlocher, M Louise" sort="Herlocher, M Louise" uniqKey="Herlocher M" first="M. Louise" last="Herlocher">M. Louise Herlocher</name></noRegion><name sortKey="Elias, Stephanie" sort="Elias, Stephanie" uniqKey="Elias S" first="Stephanie" last="Elias">Stephanie Elias</name><name sortKey="Herlocher, M Louise" sort="Herlocher, M Louise" uniqKey="Herlocher M" first="M. Louise" last="Herlocher">M. Louise Herlocher</name><name sortKey="Merry, Andrew" sort="Merry, Andrew" uniqKey="Merry A" first="Andrew" last="Merry">Andrew Merry</name><name sortKey="Monto, Arnold S" sort="Monto, Arnold S" uniqKey="Monto A" first="Arnold S." last="Monto">Arnold S. Monto</name></country><country name="Royaume-Uni"><noRegion><name sortKey="Fenton, Rob" sort="Fenton, Rob" uniqKey="Fenton R" first="Rob" last="Fenton">Rob Fenton</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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