Cooperation between the hemagglutinin of avian viruses and the matrix protein of human influenza A viruses.
Identifieur interne : 000355 ( PubMed/Curation ); précédent : 000354; suivant : 000356Cooperation between the hemagglutinin of avian viruses and the matrix protein of human influenza A viruses.
Auteurs : Christoph Scholtissek [États-Unis] ; Jürgen Stech ; Scott Krauss ; Robert G. WebsterSource :
- Journal of virology [ 0022-538X ] ; 2002.
Descripteurs français
- KwdFr :
- Amantadine (pharmacologie), Animaux, Antiviraux (pharmacologie), Chiens, Glycoprotéine hémagglutinine du virus influenza (génétique), Glycoprotéine hémagglutinine du virus influenza (métabolisme), Grippe chez les oiseaux (virologie), Grippe humaine (virologie), Humains, Lignée cellulaire, Méthode des plages virales, Protéines de la matrice virale (génétique), Protéines de la matrice virale (métabolisme), Rein (cytologie), Rein (virologie), Résistance virale aux médicaments, Virus de la grippe A (), Virus de la grippe A (croissance et développement), Virus de la grippe A (génétique), Virus de la grippe A (métabolisme), Virus recombinants, Volaille.
- MESH :
- croissance et développement : Virus de la grippe A.
- cytologie : Rein.
- génétique : Glycoprotéine hémagglutinine du virus influenza, Protéines de la matrice virale, Virus de la grippe A.
- métabolisme : Glycoprotéine hémagglutinine du virus influenza, Protéines de la matrice virale, Virus de la grippe A.
- pharmacologie : Amantadine, Antiviraux.
- virologie : Grippe chez les oiseaux, Grippe humaine, Rein.
- Animaux, Chiens, Humains, Lignée cellulaire, Méthode des plages virales, Résistance virale aux médicaments, Virus de la grippe A, Virus recombinants, Volaille.
English descriptors
- KwdEn :
- Amantadine (pharmacology), Animals, Antiviral Agents (pharmacology), Cell Line, Dogs, Drug Resistance, Viral, Hemagglutinin Glycoproteins, Influenza Virus (genetics), Hemagglutinin Glycoproteins, Influenza Virus (metabolism), Humans, Influenza A virus (drug effects), Influenza A virus (genetics), Influenza A virus (growth & development), Influenza A virus (metabolism), Influenza in Birds (virology), Influenza, Human (virology), Kidney (cytology), Kidney (virology), Poultry, Reassortant Viruses, Viral Matrix Proteins (genetics), Viral Matrix Proteins (metabolism), Viral Plaque Assay.
- MESH :
- chemical , genetics : Hemagglutinin Glycoproteins, Influenza Virus, Viral Matrix Proteins.
- chemical , metabolism : Hemagglutinin Glycoproteins, Influenza Virus, Viral Matrix Proteins.
- chemical , pharmacology : Amantadine, Antiviral Agents.
- cytology : Kidney.
- drug effects : Influenza A virus.
- genetics : Influenza A virus.
- growth & development : Influenza A virus.
- metabolism : Influenza A virus.
- virology : Influenza in Birds, Influenza, Human, Kidney.
- Animals, Cell Line, Dogs, Drug Resistance, Viral, Humans, Poultry, Reassortant Viruses, Viral Plaque Assay.
Abstract
To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning.
DOI: 10.1128/jvi.76.4.1781-1786.2002
PubMed: 11799173
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la grippe A (métabolisme)</term><term>Virus recombinants</term><term>Volaille</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Hemagglutinin Glycoproteins, Influenza Virus</term><term>Viral Matrix Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Hemagglutinin Glycoproteins, Influenza Virus</term><term>Viral Matrix Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Amantadine</term><term>Antiviral Agents</term></keywords><keywords scheme="MESH" qualifier="croissance et développement" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Rein</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Kidney</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Influenza A 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humaine</term><term>Rein</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Influenza in Birds</term><term>Influenza, Human</term><term>Kidney</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Dogs</term><term>Drug Resistance, Viral</term><term>Humans</term><term>Poultry</term><term>Reassortant Viruses</term><term>Viral Plaque Assay</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Chiens</term><term>Humains</term><term>Lignée cellulaire</term><term>Méthode des plages virales</term><term>Résistance virale aux médicaments</term><term>Virus de la grippe A</term><term>Virus recombinants</term><term>Volaille</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11799173</PMID><DateCompleted><Year>2002</Year><Month>02</Month><Day>22</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>76</Volume><Issue>4</Issue><PubDate><Year>2002</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Cooperation between the hemagglutinin of avian viruses and the matrix protein of human influenza A viruses.</ArticleTitle><Pagination><MedlinePgn>1781-6</MedlinePgn></Pagination><Abstract><AbstractText>To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Scholtissek</LastName><ForeName>Christoph</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Virology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stech</LastName><ForeName>Jürgen</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Krauss</LastName><ForeName>Scott</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Webster</LastName><ForeName>Robert G</ForeName><Initials>RG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>N01AI95357</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA021765</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI29680</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral 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Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D024882" MajorTopicYN="N">Drug Resistance, Viral</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019267" MajorTopicYN="N">Hemagglutinin Glycoproteins, Influenza Virus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009980" MajorTopicYN="N">Influenza A virus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" 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