Temperature-sensitive defect of influenza A/Ann Arbor/6/60 cold-adapted variant leads to a blockage of matrix polypeptide incorporation into the plasma membrane of the infected cells
Identifieur interne : 002402 ( Main/Merge ); précédent : 002401; suivant : 002403Temperature-sensitive defect of influenza A/Ann Arbor/6/60 cold-adapted variant leads to a blockage of matrix polypeptide incorporation into the plasma membrane of the infected cells
Auteurs : Odagiri Takato [Japon] ; Tanaka Toshinori [Japon] ; Tobita Kiyotake [Japon]Source :
- Virus Research [ 0168-1702 ] ; 1987.
English descriptors
- Teeft :
- Abortive infection, Academic press, Acrylamide, Blockage, Blood cells, Compans, Culture fluid, Electron microscopy, Host cell, Infectious virus, Infectivity, Influenza, Influenza virus, Kendal, Maassab, Mdck, Mdck cells, Membrane, Mutant, Mutation, Negative strand viruses, Odagiri, Other hand, Phenotype, Plaque assay, Plasma membranes, Polypeptide, Polypeptide content, Polypeptide incorporation, Polypeptide patterns, Polypeptide synthesis, Present study, Reassortant, Reassortants, Restrictive temperature, Rough membrane fractions, Sucrose, Tobita, Variant, Variant strain, Viral, Viral polypeptides, Virion, Virol, Virology, Virus.
Abstract
Abstract: A temperature-sensitive (ts) defect in growth of the A/Ann Arbor/6/60 (A/AA/60) cold-adapted (ca) and ts variant strain has been studied. At the restrictive temperature of 38.5°C, the variant synthesized all the viral polypeptides in normal amounts within the infected cells, but the virions released into the culture fluid contained greatly reduced amounts of the matrix (M1) polypeptide and showed significantly low infectivity per unit hemagglutinin activity. Cell fractionation experiments revealed that incorporation of the M1 polypeptide into plasma membranes of the variant-infected cells was selectively reduced at 38.5°C, whilst it occurred normally at 34°C. The ts reassortants between the A/AA/60 variant and the A/AA/1/80 wild type (wt) strain (non-ts), which had the M gene derived from the wt parent, also showed similar patterns. These results suggest that the ts defect of the variant and its ts reassortants involves the process of incorporation of the M1 polypeptide into the plasma membranes of the infected cells and that this defect is not attributable to the M gene of the variant.
Url:
DOI: 10.1016/0168-1702(87)90028-1
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329-04</wicri:regionArea><wicri:noRegion>Tochigi 329-04</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Virus Research</title><title level="j" type="abbrev">VIRUS</title><idno type="ISSN">0168-1702</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1987">1987</date><biblScope unit="volume">7</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="203">203</biblScope><biblScope unit="page" to="218">218</biblScope></imprint><idno type="ISSN">0168-1702</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0168-1702</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abortive infection</term><term>Academic press</term><term>Acrylamide</term><term>Blockage</term><term>Blood cells</term><term>Compans</term><term>Culture fluid</term><term>Electron microscopy</term><term>Host cell</term><term>Infectious virus</term><term>Infectivity</term><term>Influenza</term><term>Influenza virus</term><term>Kendal</term><term>Maassab</term><term>Mdck</term><term>Mdck cells</term><term>Membrane</term><term>Mutant</term><term>Mutation</term><term>Negative strand viruses</term><term>Odagiri</term><term>Other hand</term><term>Phenotype</term><term>Plaque assay</term><term>Plasma membranes</term><term>Polypeptide</term><term>Polypeptide content</term><term>Polypeptide incorporation</term><term>Polypeptide patterns</term><term>Polypeptide synthesis</term><term>Present study</term><term>Reassortant</term><term>Reassortants</term><term>Restrictive temperature</term><term>Rough membrane fractions</term><term>Sucrose</term><term>Tobita</term><term>Variant</term><term>Variant strain</term><term>Viral</term><term>Viral polypeptides</term><term>Virion</term><term>Virol</term><term>Virology</term><term>Virus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: A temperature-sensitive (ts) defect in growth of the A/Ann Arbor/6/60 (A/AA/60) cold-adapted (ca) and ts variant strain has been studied. At the restrictive temperature of 38.5°C, the variant synthesized all the viral polypeptides in normal amounts within the infected cells, but the virions released into the culture fluid contained greatly reduced amounts of the matrix (M1) polypeptide and showed significantly low infectivity per unit hemagglutinin activity. Cell fractionation experiments revealed that incorporation of the M1 polypeptide into plasma membranes of the variant-infected cells was selectively reduced at 38.5°C, whilst it occurred normally at 34°C. The ts reassortants between the A/AA/60 variant and the A/AA/1/80 wild type (wt) strain (non-ts), which had the M gene derived from the wt parent, also showed similar patterns. These results suggest that the ts defect of the variant and its ts reassortants involves the process of incorporation of the M1 polypeptide into the plasma membranes of the infected cells and that this defect is not attributable to the M gene of the variant.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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