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.
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 degrees 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 degrees C, whilst it occurred normally at 34 degrees 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.
D001692:Biological Transport; D002462:Cell Membrane / Q000378:metabolism; D003593:Cytoplasm / Q000378:metabolism; D009980:Influenza A virus / Q000235:genetics* / Q000648:ultrastructure; D009154:Mutation; D010641:Phenotype; D013696:Temperature; D014763:Viral Matrix Proteins; D014764:Viral Proteins / Q000378:metabolism*; D014779:Virus Replication
D014763:Viral Matrix Proteins; D014764:Viral Proteins