A reassortant between influenza A viruses (H7N2) synthesizing an enzymatically inactive neuraminidase at 40° which is not incorporated into infectious particles
Identifieur interne : 002386 ( Main/Exploration ); précédent : 002385; suivant : 002387A reassortant between influenza A viruses (H7N2) synthesizing an enzymatically inactive neuraminidase at 40° which is not incorporated into infectious particles
Auteurs : Astrid Breuning [Allemagne] ; Christoph Scholtissek [Allemagne]Source :
- Virology [ 0042-6822 ] ; 1986.
English descriptors
- Teeft :
- Academic press, Beckman instruments, Blood cells, Body temperature, Breuning, Carbohydrate side chains, Chick embryo cells, Complex types, Cytoplasmic membrane, Enzyme activity, Fraction fraction, Glycoprotein, Golgi bodies, Hemagglutinating activity, Hong kong parent virus, Hong kong virus, Infectious particles, Influenza, Influenza virus, Influenza virus replication, Influenza viruses, Klenk, Lanes cells, Lower panel, Lysis buffer, Mannose type, Membrane, Membrane fusion, Membranes mixture, Neuraminidase, Neuraminidase activity, Nonreducing conditions, Normal yields, Oligosaccharide, Oligosaccharide peptides, Optical density, Other genes, Other reassortants, Parent viruses, Permissive temperature, Reassortant, Reassortants, Rough endoplasmic reticulum, Rough membranes, Same position, Scholtissek, Smooth membranes, Sucrose, Surface glycoprotein composition, Thorough digestion, Various fractions, Viral, Viral glycoproteins, Viral particles, Virology, Virus particles, Virus release, Virus strains, Viruses table.
Abstract
Abstract: Cells infected with a reassortant (113/Ho, H7N2) between A/fowl plague/Rostock/34 (FPV, H7N1) and A/Hong Kong/1/68 (H3N2) carrying RNA segments 1 and 6 of the Hong Kong virus and the residual genes of FPV, synthesized at 40° a neuraminidase (NA) which is enzymatically not active and which is not incorporated into infectious particles. At 40° NA accumulates in the rough endoplasmic reticulum. It contains mainly carbohydrate side chains of the mannose type, and fucose is only scarcely incorporated. At 33° NA of the reassortant is overproduced, and at least some of it is active and is incorporated into viral particles. Under nonreducing conditions during PAGE its NA migrates to the same position as after heating with mercaptoethanol, in contrast to the Hong Kong parent virus. It is speculated that at 40° the tetramerization of the NA in the rough endoplasmic reticulum does not function, and in this way its migration to the cytoplasmic membrane and its incorporation into infectious particles does not occur. Since 113/Ho is as pathogenic for the chicken (body temperature of 41°) as is FPV, the question arises which role the NA plays in virus replication and spread in the infected organism.
Url:
DOI: 10.1016/0042-6822(86)90266-7
Affiliations:
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ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Cells infected with a reassortant (113/Ho, H7N2) between A/fowl plague/Rostock/34 (FPV, H7N1) and A/Hong Kong/1/68 (H3N2) carrying RNA segments 1 and 6 of the Hong Kong virus and the residual genes of FPV, synthesized at 40° a neuraminidase (NA) which is enzymatically not active and which is not incorporated into infectious particles. At 40° NA accumulates in the rough endoplasmic reticulum. It contains mainly carbohydrate side chains of the mannose type, and fucose is only scarcely incorporated. At 33° NA of the reassortant is overproduced, and at least some of it is active and is incorporated into viral particles. Under nonreducing conditions during PAGE its NA migrates to the same position as after heating with mercaptoethanol, in contrast to the Hong Kong parent virus. It is speculated that at 40° the tetramerization of the NA in the rough endoplasmic reticulum does not function, and in this way its migration to the cytoplasmic membrane and its incorporation into infectious particles does not occur. Since 113/Ho is as pathogenic for the chicken (body temperature of 41°) as is FPV, the question arises which role the NA plays in virus replication and spread in the infected organism.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Breuning, Astrid" sort="Breuning, Astrid" uniqKey="Breuning A" first="Astrid" last="Breuning">Astrid Breuning</name></noRegion><name sortKey="Scholtissek, Christoph" sort="Scholtissek, Christoph" uniqKey="Scholtissek C" first="Christoph" last="Scholtissek">Christoph Scholtissek</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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