Genetic basis of resistance to rimantadine emerging during treatment of influenza virus infection.
Identifieur interne : 001063 ( Ncbi/Curation ); précédent : 001062; suivant : 001064Genetic basis of resistance to rimantadine emerging during treatment of influenza virus infection.
Auteurs : R B Belshe [Royaume-Uni] ; M H Smith ; C B Hall ; R. Betts ; A J HaySource :
- Journal of virology [ 0022-538X ] ; 1988.
Descripteurs français
- KwdFr :
- Adamantane (analogues et dérivés), Données de séquences moléculaires, Essais cliniques comme sujet, Grippe humaine (traitement médicamenteux), Humains, Rimantadine (usage thérapeutique), Résistance microbienne aux médicaments (génétique), Séquence d'acides aminés, Séquence nucléotidique, Virus de la grippe A (), Virus de la grippe A (génétique).
- MESH :
- analogues et dérivés : Adamantane.
- génétique : Résistance microbienne aux médicaments, Virus de la grippe A.
- traitement médicamenteux : Grippe humaine.
- usage thérapeutique : Rimantadine.
- Données de séquences moléculaires, Essais cliniques comme sujet, Humains, Séquence d'acides aminés, Séquence nucléotidique, Virus de la grippe A.
English descriptors
- KwdEn :
- MESH :
- chemical , analogs & derivatives : Adamantane.
- drug effects : Influenza A virus.
- drug therapy : Influenza, Human.
- genetics : Drug Resistance, Microbial, Influenza A virus.
- chemical , therapeutic use : Rimantadine.
- Amino Acid Sequence, Base Sequence, Clinical Trials as Topic, Humans, Molecular Sequence Data.
Abstract
The emergence of influenza A viruses which had acquired resistance to rimantadine during a clinical trial (C. B. Hall, R. Dolin, C. L. Gala, D. M. Markovitz, Y. Q. Zhang, P. H. Madore, F. A. Disney, W. B. Talpey, J. L. Green, A. B. Francis, and M. E. Pichichero, Pediatrics 80:275-282, 1987) provided the opportunity to determine the genetic basis of this phenomenon. Analysis of reassortant viruses generated with a resistant clinical isolate (H3N2) and the susceptible influenza A/Singapore/57 (H2N2) virus indicated that RNA segment 7 coding for matrix and M2 proteins conferred the resistant phenotype. Resistant viruses isolated from seven patients each contained a single change in the nucleotide sequence coding for the M2 protein which resulted in substitutions in amino acid 30 (two viruses) or 31 (five viruses) in the transmembrane domain of the molecule. These changes occurred in locations identified in influenza viruses selected for resistance to amantadine in tissue culture and indicate a common mechanism of action of the two compounds in cell culture and during chemotherapeutic use.
PubMed: 3282079
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Betts</name></author><author><name sortKey="Hay, A J" sort="Hay, A J" uniqKey="Hay A" first="A J" last="Hay">A J Hay</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="1988" type="published">1988</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adamantane (analogs & derivatives)</term><term>Amino Acid Sequence</term><term>Base Sequence</term><term>Clinical Trials as Topic</term><term>Drug Resistance, Microbial (genetics)</term><term>Humans</term><term>Influenza A virus (drug effects)</term><term>Influenza A virus (genetics)</term><term>Influenza, Human (drug therapy)</term><term>Molecular Sequence Data</term><term>Rimantadine (therapeutic use)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adamantane (analogues et dérivés)</term><term>Données de séquences moléculaires</term><term>Essais cliniques comme sujet</term><term>Grippe humaine (traitement médicamenteux)</term><term>Humains</term><term>Rimantadine (usage thérapeutique)</term><term>Résistance microbienne aux médicaments (génétique)</term><term>Séquence d'acides aminés</term><term>Séquence nucléotidique</term><term>Virus de la grippe A ()</term><term>Virus de la grippe A (génétique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adamantane</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Adamantane</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Drug Resistance, Microbial</term><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Résistance microbienne aux médicaments</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Rimantadine</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Rimantadine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Base Sequence</term><term>Clinical Trials as Topic</term><term>Humans</term><term>Molecular Sequence Data</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Données de séquences moléculaires</term><term>Essais cliniques comme sujet</term><term>Humains</term><term>Séquence d'acides aminés</term><term>Séquence nucléotidique</term><term>Virus de la grippe A</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The emergence of influenza A viruses which had acquired resistance to rimantadine during a clinical trial (C. B. Hall, R. Dolin, C. L. Gala, D. M. Markovitz, Y. Q. Zhang, P. H. Madore, F. A. Disney, W. B. Talpey, J. L. Green, A. B. Francis, and M. E. Pichichero, Pediatrics 80:275-282, 1987) provided the opportunity to determine the genetic basis of this phenomenon. Analysis of reassortant viruses generated with a resistant clinical isolate (H3N2) and the susceptible influenza A/Singapore/57 (H2N2) virus indicated that RNA segment 7 coding for matrix and M2 proteins conferred the resistant phenotype. Resistant viruses isolated from seven patients each contained a single change in the nucleotide sequence coding for the M2 protein which resulted in substitutions in amino acid 30 (two viruses) or 31 (five viruses) in the transmembrane domain of the molecule. These changes occurred in locations identified in influenza viruses selected for resistance to amantadine in tissue culture and indicate a common mechanism of action of the two compounds in cell culture and during chemotherapeutic use.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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