H2N2V1, Main, Exploration, bibRecord, 001824

Mechanisms of differential induction of apoptosis by H3N2 and H1N1 influenza viruses

Identifieur interne : 001824 ( Main/Exploration ); précédent : 001823; suivant : 001825

Mechanisms of differential induction of apoptosis by H3N2 and H1N1 influenza viruses

Auteurs : Clive Sweet [Royaume-Uni] ; Susan J. Morris [Royaume-Uni] ; Mustafa A. Mohsin [Royaume-Uni] ; Harry Smith [Royaume-Uni]

Source :

International congress series [ 0531-5131 ] ; 2001.

RBID : ISTEX:D4A0E47B29230848CFF2E8B4FDFCDAE006B6BF69

English descriptors

Teeft :
- Apoptosis, Avian, Clone, Differential induction, Elsevier science, Erythrocyte, Expression vectors, Fluorescence staining, Fusion proteins, Glycosylation, Good correlation, Hela, Hela cells, Hemagglutinin, Horse serum, Influenza, Influenza apoptosis, Influenza virus, Influenza virus genes, Influenza viruses, International congress series, Invitrogen voyager2 vector, Mdck, Mdck cells, Monoclonal antibody, Neuraminidase, Oligosaccharide, Poly, Possible explanation, Potential glycosylation sites, Receptor, Receptor binding site, Room temperature, Standard deviation, Transfected, Transfected cells, Transfection, Transient transfection assays, Virol, Virology, Virus, Viruses clone.

Abstract

Abstract: Background: The abilities of seven H3N2 and four H1N1 influenza viruses to infect MDCK cells and produce apoptosis were measured and related to their neuraminidase (NA) activity and the role of individual influenza virus proteins in induction of apoptosis was also investigated by transient transfection assays in HeLa cells with expression vectors containing individual virus genes. Methods: MDCK cells were inoculated at a high multiplicity of infection (5 EID50/cell) and apoptosis was measured by cytotoxicity and morphology while infection was quantified by fluorescence staining with anti-nucleoprotein (NP) antibody. The Invitrogen Voyager™ vector expressing influenza virus genes as VP22 fusion proteins was transfected into HeLa cells using lipofectamine. Results and discussion: H3N2 viruses with high NA activities (1.4–1.8 μmol/l/min) induced high levels of apoptosis (83–94%) and infected 91–98% of cells, while H1N1 viruses with low NA activities (0.22–0.33 μmol/l/min) were poor apoptosis inducers (11–19%) and infected few (15–21%) cells. The differences in % infected cells reflected differences in haemagglutinin (HA) receptor binding affinity. Treatment of viruses with bacterial NA to remove sialyl groups from oligosaccharides on virus HA increased their ability to infect MDCK cells and the increase correlated inversely with the number of potential glycosylation sites around the receptor binding site. Transfection experiments showed that NA (from clone 7a but not A/Fiji) and NS1 (from clone 7a and A/Fiji) induced apoptosis, while NP (clone 7a and A/Fiji) did not.

Url:

https://api.istex.fr/ark:/67375/6H6-M3KJKSZ3-1/fulltext.pdf

DOI: 10.1016/S0531-5131(01)00636-7

Affiliations:

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Le document en format XML

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<term>Influenza viruses</term>
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<term>Monoclonal antibody</term>
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<term>Poly</term>
<term>Possible explanation</term>
<term>Potential glycosylation sites</term>
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<term>Transfected cells</term>
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<front><div type="abstract" xml:lang="en">Abstract: Background: The abilities of seven H3N2 and four H1N1 influenza viruses to infect MDCK cells and produce apoptosis were measured and related to their neuraminidase (NA) activity and the role of individual influenza virus proteins in induction of apoptosis was also investigated by transient transfection assays in HeLa cells with expression vectors containing individual virus genes. Methods: MDCK cells were inoculated at a high multiplicity of infection (5 EID50/cell) and apoptosis was measured by cytotoxicity and morphology while infection was quantified by fluorescence staining with anti-nucleoprotein (NP) antibody. The Invitrogen Voyager™ vector expressing influenza virus genes as VP22 fusion proteins was transfected into HeLa cells using lipofectamine. Results and discussion: H3N2 viruses with high NA activities (1.4–1.8 μmol/l/min) induced high levels of apoptosis (83–94%) and infected 91–98% of cells, while H1N1 viruses with low NA activities (0.22–0.33 μmol/l/min) were poor apoptosis inducers (11–19%) and infected few (15–21%) cells. The differences in % infected cells reflected differences in haemagglutinin (HA) receptor binding affinity. Treatment of viruses with bacterial NA to remove sialyl groups from oligosaccharides on virus HA increased their ability to infect MDCK cells and the increase correlated inversely with the number of potential glycosylation sites around the receptor binding site. Transfection experiments showed that NA (from clone 7a but not A/Fiji) and NS1 (from clone 7a and A/Fiji) induced apoptosis, while NP (clone 7a and A/Fiji) did not.</div>
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Mechanisms of differential induction of apoptosis by H3N2 and H1N1 influenza viruses

Mechanisms of differential induction of apoptosis by H3N2 and H1N1 influenza viruses

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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