Antibodies to HA and NA augment uptake of influenza A viruses into cells via Fc receptor entry
Identifieur interne : 002034 ( Main/Curation ); précédent : 002033; suivant : 002035Antibodies to HA and NA augment uptake of influenza A viruses into cells via Fc receptor entry
Auteurs : Manabu Tamura [États-Unis] ; Robert G. Webster [États-Unis] ; Francis A. Ennis [États-Unis]Source :
- Virology [ 0042-6822 ] ; 1991.
English descriptors
- Teeft :
- Academic press, Antibody responses, Antigenic, Antigenic drift, Antigenic sites, Antigenic variation, Binding buffer, Cell line, Cell responses, Column volumes, Cytoplasmic preparations, Dengue virus infection, Dilution, Enhancement, Enhancement antigens, Ennis, Hybridization, Hybridization analysis, Hybridization technique, Immune, Immune responses, Immune serum, Immunofluorescence, Indirect immunofluorescence staining, Infection, Infectious virus, Influenza, Influenza antigens, Influenza avirus infection, Influenza complexes, Influenza infection, Influenza virus, Influenza virus cells, Internal antigens, Internal genes, Lower dilutions, Lower serum dilutions, Lymphocyte, Macrophage, Monoclonal, Monoclonal antibodies, Monoclonal antibody, Mouse polyclonal, Mouse serum, Mrna, Murine, Murine polyclonal, Neuraminidase, Neutralization, Neutralizing, Neutralizing activity, Neutralizing antigens, Nonneutralizing antibodies, Other hand, Polyclonal, Reassortant, Reassortant viruses, Receptor, Results show, Sialic acid residues, Sodium acetate, Specific antisera, Specific goat antisera, Various concentrations, Various dilutions, Viral, Viral antigens, Virus, Virus infection, Virus receptors, Virus strains, Virus uptake, Yellow fever virus.
Abstract
Abstract: The hemagglutinin (HA) and neuraminidase (NA) of influenza A viruses induce antibodies which augment the uptake of influenza A virus by antigen presenting cells via Fc receptor entry. Antibody-dependent enhancement of uptake of virus by cells was mediated by Fc receptors because F(ab′)2 preparations of IgG mixed with virus did not enhance virus uptake. This enhanced infection was measured using a fluorescent focus assay and was confirmed by dot-blot hybridization analysis. A 25-fold increase in the number of cells containing influenza antigens was detected when virus was mixed with subneutralizing concentrations of immune serum to the homologous virus before adding to neuraminidase-treated cells. Infection was also augmented using reassortant viruses which shared only the HA or the NA of the virus used to induce antibodies. Specific antisera to purified HA or NA also enhanced virus uptake. These results indicate that both the HA and the NA induce antibodies that enhance uptake of virus by Fc receptor bearing cells. In addition we determined that the drift of neutralizing antigens occurred more quickly than the drift of infection-enhancing antigens during the evolution of virus strains of the H3 subtype. The increase in the number of antigen presenting cells as a result of uptake of virus complexed with cross-reactive enhancing antibodies may affect the T cell responses to influenza infection.
Url:
DOI: 10.1016/0042-6822(91)90664-W
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Webster</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Virology, St. Jude Children's Research Hospital, 322 N. Lauderdale, P. O. Box 318, Memphis, Tennessee 38101</wicri:regionArea><wicri:noRegion>Tennessee 38101</wicri:noRegion></affiliation></author><author><name sortKey="Ennis, Francis A" sort="Ennis, Francis A" uniqKey="Ennis F" first="Francis A." last="Ennis">Francis A. Ennis</name><affiliation></affiliation><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Infectious Diseases, Department of Medicine, University of Massachusetts Medical Center, Worcester, Massachusetts 01655</wicri:regionArea><wicri:noRegion>Massachusetts 01655</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">182</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="211">211</biblScope><biblScope unit="page" to="219">219</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Academic press</term><term>Antibody responses</term><term>Antigenic</term><term>Antigenic drift</term><term>Antigenic sites</term><term>Antigenic variation</term><term>Binding buffer</term><term>Cell line</term><term>Cell responses</term><term>Column volumes</term><term>Cytoplasmic preparations</term><term>Dengue virus infection</term><term>Dilution</term><term>Enhancement</term><term>Enhancement antigens</term><term>Ennis</term><term>Hybridization</term><term>Hybridization analysis</term><term>Hybridization technique</term><term>Immune</term><term>Immune responses</term><term>Immune serum</term><term>Immunofluorescence</term><term>Indirect immunofluorescence staining</term><term>Infection</term><term>Infectious virus</term><term>Influenza</term><term>Influenza antigens</term><term>Influenza avirus infection</term><term>Influenza complexes</term><term>Influenza infection</term><term>Influenza virus</term><term>Influenza virus cells</term><term>Internal antigens</term><term>Internal genes</term><term>Lower dilutions</term><term>Lower serum dilutions</term><term>Lymphocyte</term><term>Macrophage</term><term>Monoclonal</term><term>Monoclonal antibodies</term><term>Monoclonal antibody</term><term>Mouse polyclonal</term><term>Mouse serum</term><term>Mrna</term><term>Murine</term><term>Murine polyclonal</term><term>Neuraminidase</term><term>Neutralization</term><term>Neutralizing</term><term>Neutralizing activity</term><term>Neutralizing antigens</term><term>Nonneutralizing antibodies</term><term>Other hand</term><term>Polyclonal</term><term>Reassortant</term><term>Reassortant viruses</term><term>Receptor</term><term>Results show</term><term>Sialic acid residues</term><term>Sodium acetate</term><term>Specific antisera</term><term>Specific goat antisera</term><term>Various concentrations</term><term>Various dilutions</term><term>Viral</term><term>Viral antigens</term><term>Virus</term><term>Virus infection</term><term>Virus receptors</term><term>Virus strains</term><term>Virus uptake</term><term>Yellow fever virus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The hemagglutinin (HA) and neuraminidase (NA) of influenza A viruses induce antibodies which augment the uptake of influenza A virus by antigen presenting cells via Fc receptor entry. Antibody-dependent enhancement of uptake of virus by cells was mediated by Fc receptors because F(ab′)2 preparations of IgG mixed with virus did not enhance virus uptake. This enhanced infection was measured using a fluorescent focus assay and was confirmed by dot-blot hybridization analysis. A 25-fold increase in the number of cells containing influenza antigens was detected when virus was mixed with subneutralizing concentrations of immune serum to the homologous virus before adding to neuraminidase-treated cells. Infection was also augmented using reassortant viruses which shared only the HA or the NA of the virus used to induce antibodies. Specific antisera to purified HA or NA also enhanced virus uptake. These results indicate that both the HA and the NA induce antibodies that enhance uptake of virus by Fc receptor bearing cells. In addition we determined that the drift of neutralizing antigens occurred more quickly than the drift of infection-enhancing antigens during the evolution of virus strains of the H3 subtype. The increase in the number of antigen presenting cells as a result of uptake of virus complexed with cross-reactive enhancing antibodies may affect the T cell responses to influenza infection.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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