Subtype cross-reactive, infection-enhancing antibody responses to influenza A viruses.
Identifieur interne : 000376 ( PubMed/Checkpoint ); précédent : 000375; suivant : 000377Subtype cross-reactive, infection-enhancing antibody responses to influenza A viruses.
Auteurs : M. Tamura ; R G Webster ; F A EnnisSource :
- Journal of virology [ 0022-538X ] ; 1994.
Descripteurs français
- KwdFr :
- Animaux, Anticorps antiviraux (biosynthèse), Anticorps monoclonaux, Antigènes viraux, Cellules présentatrices d'antigène (immunologie), Cellules présentatrices d'antigène (microbiologie), Grippe humaine (enzymologie), Grippe humaine (immunologie), Grippe humaine (microbiologie), Humains, Lignée cellulaire, Mâle, Réactions croisées, Récepteur Fc (métabolisme), Sialidase (immunologie), Souris, Souris de lignée BALB C, Tests de neutralisation, Virus de la grippe A (), Virus de la grippe A (immunologie).
- MESH :
- biosynthèse : Anticorps antiviraux.
- enzymologie : Grippe humaine.
- immunologie : Cellules présentatrices d'antigène, Grippe humaine, Sialidase, Virus de la grippe A.
- microbiologie : Cellules présentatrices d'antigène, Grippe humaine.
- métabolisme : Récepteur Fc.
- Animaux, Anticorps monoclonaux, Antigènes viraux, Humains, Lignée cellulaire, Mâle, Réactions croisées, Souris, Souris de lignée BALB C, Tests de neutralisation, Virus de la grippe A.
English descriptors
- KwdEn :
- Animals, Antibodies, Monoclonal, Antibodies, Viral (biosynthesis), Antigen-Presenting Cells (immunology), Antigen-Presenting Cells (microbiology), Antigens, Viral, Cell Line, Cross Reactions, Humans, Influenza A virus (classification), Influenza A virus (immunology), Influenza, Human (enzymology), Influenza, Human (immunology), Influenza, Human (microbiology), Male, Mice, Mice, Inbred BALB C, Neuraminidase (immunology), Neutralization Tests, Receptors, Fc (metabolism).
- MESH :
- chemical , biosynthesis : Antibodies, Viral.
- chemical , immunology : Neuraminidase.
- chemical , metabolism : Receptors, Fc.
- chemical : Antibodies, Monoclonal, Antigens, Viral.
- classification : Influenza A virus.
- enzymology : Influenza, Human.
- immunology : Antigen-Presenting Cells, Influenza A virus, Influenza, Human.
- microbiology : Antigen-Presenting Cells, Influenza, Human.
- Animals, Cell Line, Cross Reactions, Humans, Male, Mice, Mice, Inbred BALB C, Neutralization Tests.
Abstract
Antibody-dependent enhancement of the uptake of influenza A virus by Fc receptor-bearing cells was analyzed by using virus strains of the three human influenza A virus subtypes, A/PR/8/34 (H1N1), A/Japan/305/57 (H2N2), and A/Port Chalmers/1/73 (H3N2). Immune sera obtained from mice following primary infection with an H1N1, H2N2, or H3N2 subtype virus neutralized only virus of the same subtype; however, immune sera augmented the uptake of virus across subtypes. Immune sera from H1N1-infected mice augmented uptake of the homologous (H1N1) and H2N2 viruses. Antisera to the H2N2 virus augmented the uptake of virus of all subtypes (H1N1, H2N2, or H3N2). Antisera to the H3N2 virus augmented the uptake of the homologous (H3N2) and H2N2 viruses. These results show that subtype cross-reactive, nonneutralizing antibodies augment the uptake of influenza A virus strains of different subtypes. Antibodies to neuraminidase may contribute to the enhanced uptake of viruses of a different subtype, because N2-specific monoclonal antibodies augmented the uptake of both A/Japan/305/57 (H2N2) and A/Port Chalmers/1/73 (H3N2) viruses.
PubMed: 8189489
Affiliations:
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Tamura</name><affiliation><nlm:affiliation>Department of Medicine, University of Massachusetts Medical Center, Worcester 01655.</nlm:affiliation><wicri:noCountry code="subField">Worcester 01655</wicri:noCountry></affiliation></author><author><name sortKey="Webster, R G" sort="Webster, R G" uniqKey="Webster R" first="R G" last="Webster">R G Webster</name></author><author><name sortKey="Ennis, F A" sort="Ennis, F A" uniqKey="Ennis F" first="F A" last="Ennis">F A Ennis</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1994">1994</date><idno type="RBID">pubmed:8189489</idno><idno type="pmid">8189489</idno><idno type="wicri:Area/PubMed/Corpus">000416</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000416</idno><idno type="wicri:Area/PubMed/Curation">000416</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000416</idno><idno type="wicri:Area/PubMed/Checkpoint">000376</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000376</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Subtype cross-reactive, infection-enhancing antibody responses to influenza A viruses.</title><author><name sortKey="Tamura, M" sort="Tamura, M" uniqKey="Tamura M" first="M" last="Tamura">M. Tamura</name><affiliation><nlm:affiliation>Department of Medicine, University of Massachusetts Medical Center, Worcester 01655.</nlm:affiliation><wicri:noCountry code="subField">Worcester 01655</wicri:noCountry></affiliation></author><author><name sortKey="Webster, R G" sort="Webster, R G" uniqKey="Webster R" first="R G" last="Webster">R G Webster</name></author><author><name sortKey="Ennis, F A" sort="Ennis, F A" uniqKey="Ennis F" first="F A" last="Ennis">F A Ennis</name></author></analytic><series><title level="j">Journal of virology</title><idno type="ISSN">0022-538X</idno><imprint><date when="1994" type="published">1994</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Monoclonal</term><term>Antibodies, Viral (biosynthesis)</term><term>Antigen-Presenting Cells (immunology)</term><term>Antigen-Presenting Cells (microbiology)</term><term>Antigens, Viral</term><term>Cell Line</term><term>Cross Reactions</term><term>Humans</term><term>Influenza A virus (classification)</term><term>Influenza A virus (immunology)</term><term>Influenza, Human (enzymology)</term><term>Influenza, Human (immunology)</term><term>Influenza, Human (microbiology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Neuraminidase (immunology)</term><term>Neutralization Tests</term><term>Receptors, Fc (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anticorps antiviraux (biosynthèse)</term><term>Anticorps monoclonaux</term><term>Antigènes viraux</term><term>Cellules présentatrices d'antigène (immunologie)</term><term>Cellules présentatrices d'antigène (microbiologie)</term><term>Grippe humaine (enzymologie)</term><term>Grippe humaine (immunologie)</term><term>Grippe humaine (microbiologie)</term><term>Humains</term><term>Lignée cellulaire</term><term>Mâle</term><term>Réactions croisées</term><term>Récepteur Fc (métabolisme)</term><term>Sialidase (immunologie)</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Tests de neutralisation</term><term>Virus de la grippe A ()</term><term>Virus de la grippe A (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Antibodies, Viral</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Neuraminidase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Fc</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Antibodies, Monoclonal</term><term>Antigens, Viral</term></keywords><keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Anticorps antiviraux</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules présentatrices d'antigène</term><term>Grippe humaine</term><term>Sialidase</term><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Antigen-Presenting Cells</term><term>Influenza A virus</term><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Cellules présentatrices d'antigène</term><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Antigen-Presenting Cells</term><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Récepteur Fc</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line</term><term>Cross Reactions</term><term>Humans</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Neutralization Tests</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Anticorps monoclonaux</term><term>Antigènes viraux</term><term>Humains</term><term>Lignée cellulaire</term><term>Mâle</term><term>Réactions croisées</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Tests de neutralisation</term><term>Virus de la grippe A</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antibody-dependent enhancement of the uptake of influenza A virus by Fc receptor-bearing cells was analyzed by using virus strains of the three human influenza A virus subtypes, A/PR/8/34 (H1N1), A/Japan/305/57 (H2N2), and A/Port Chalmers/1/73 (H3N2). Immune sera obtained from mice following primary infection with an H1N1, H2N2, or H3N2 subtype virus neutralized only virus of the same subtype; however, immune sera augmented the uptake of virus across subtypes. Immune sera from H1N1-infected mice augmented uptake of the homologous (H1N1) and H2N2 viruses. Antisera to the H2N2 virus augmented the uptake of virus of all subtypes (H1N1, H2N2, or H3N2). Antisera to the H3N2 virus augmented the uptake of the homologous (H3N2) and H2N2 viruses. These results show that subtype cross-reactive, nonneutralizing antibodies augment the uptake of influenza A virus strains of different subtypes. Antibodies to neuraminidase may contribute to the enhanced uptake of viruses of a different subtype, because N2-specific monoclonal antibodies augmented the uptake of both A/Japan/305/57 (H2N2) and A/Port Chalmers/1/73 (H3N2) viruses.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8189489</PMID><DateCompleted><Year>1994</Year><Month>06</Month><Day>20</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>68</Volume><Issue>6</Issue><PubDate><Year>1994</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Subtype cross-reactive, infection-enhancing antibody responses to influenza A viruses.</ArticleTitle><Pagination><MedlinePgn>3499-504</MedlinePgn></Pagination><Abstract><AbstractText>Antibody-dependent enhancement of the uptake of influenza A virus by Fc receptor-bearing cells was analyzed by using virus strains of the three human influenza A virus subtypes, A/PR/8/34 (H1N1), A/Japan/305/57 (H2N2), and A/Port Chalmers/1/73 (H3N2). Immune sera obtained from mice following primary infection with an H1N1, H2N2, or H3N2 subtype virus neutralized only virus of the same subtype; however, immune sera augmented the uptake of virus across subtypes. Immune sera from H1N1-infected mice augmented uptake of the homologous (H1N1) and H2N2 viruses. Antisera to the H2N2 virus augmented the uptake of virus of all subtypes (H1N1, H2N2, or H3N2). Antisera to the H3N2 virus augmented the uptake of the homologous (H3N2) and H2N2 viruses. These results show that subtype cross-reactive, nonneutralizing antibodies augment the uptake of influenza A virus strains of different subtypes. Antibodies to neuraminidase may contribute to the enhanced uptake of viruses of a different subtype, because N2-specific monoclonal antibodies augmented the uptake of both A/Japan/305/57 (H2N2) and A/Port Chalmers/1/73 (H3N2) viruses.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tamura</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Massachusetts Medical Center, Worcester 01655.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Webster</LastName><ForeName>R G</ForeName><Initials>RG</Initials></Author><Author ValidYN="Y"><LastName>Ennis</LastName><ForeName>F A</ForeName><Initials>FA</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J 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