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10.1016/0168-1702(96)01329-9 http://scihub22266oqcxt.onion/10.1016/0168-1702(96)01329-9 8879138!ä!8879138 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=8879138&cmd=llinks): Failed to open stream: HTTP request failed! 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Mutations in the hemagglutinin and matrix genes of a virulent influenza virus variant, A/FM/1/47-MA, control different stages in pathogenesis |pdf=|usr=}}{{8879138}} gab.com Text Mutations in the hemagglutinin and matrix genes of a virulent influenza virus variant, A/FM/1/47-MA, control different stages in pathogenesis JO: Virus Res http://www.kidney.de/pget.php?&tw=1&pmid=8879138 #FOAvip The mouse adapted strain of influenza A/FM/1/47 virus, FM-MA, has increased virulence due to mutations in HA, M1 and at least one other, unmapped, genome segment. Genetic reassortants that differ due to the HA or M1 mutations were used to define the role of these mutations in pathogenesis. Pathological changes in lungs of infected mice were assessed by hematoxylin phloxine saffron (HPS) staining, and viral infection was measured by fluorescent antibody staining of thin sections and flow cytometry of lung parenchymal cells. HA played a role in bronchiolar pathology by increasing necrosis of bronchiolar epithelium, peribronchiolar lymphocytes, and airway obstruction. The HA mutation was shown to be responsible for a 0.2 unit decreased in the pH optimum of fusion and controlled resistance to alpha and beta inhibitors of hemagglutination. Both these changes in biology may confer a replicative advantage in bronchioles seen in the first day of infection. Thus the HA mutation may have conferred a survival advantage in the extracellular lung environment. The M1 mutation resulted in improved growth in the lung and cultured cells and was associated with increases in recruitment of macrophages, spread of infection into the alveoli of the lung and interstitial pneumonia. Sequence analysis indicated that the unmapped mutation in the control of FM-MA virulence is either the K482-->R substitution in the PB2 protein or the D538-->G substitution in the PB1 protein. One or other of these mutations results in a growth advantage in infected lung but not in cultured cells as well as a further increased recruitment and infection of macrophages in the lung. Infection with virulent strains of influenza that induced increases in macrophage recruitment caused hypothermia in the mouse. Twit Text FOAVip Mutations in the hemagglutinin and matrix genes of a virulent influenza virus variant, A/FM/1/47-MA, control different stages in pathogenesis ????Virus Res http://www.kidney.de/pget.php?&tw=1&pmid=8879138 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=8879138 #FOAvip English Wikipedia <ref>{{Cite pmid|8879138}}</ref> Mutations in the hemagglutinin and matrix genes of a virulent influenza virus variant, A/FM/1/47-MA, control different stages in pathogenesis #MMPMID8879138 Smeenk CA; Wright KE; Burns BF; Thaker AJ; Brown EG Virus Res 1996[Oct]; 44 (2): 79-95 PMID8879138show ga The mouse adapted strain of influenza A/FM/1/47 virus, FM-MA, has increased virulence due to mutations in HA, M1 and at least one other, unmapped, genome segment. Genetic reassortants that differ due to the HA or M1 mutations were used to define the role of these mutations in pathogenesis. Pathological changes in lungs of infected mice were assessed by hematoxylin phloxine saffron (HPS) staining, and viral infection was measured by fluorescent antibody staining of thin sections and flow cytometry of lung parenchymal cells. HA played a role in bronchiolar pathology by increasing necrosis of bronchiolar epithelium, peribronchiolar lymphocytes, and airway obstruction. The HA mutation was shown to be responsible for a 0.2 unit decreased in the pH optimum of fusion and controlled resistance to alpha and beta inhibitors of hemagglutination. Both these changes in biology may confer a replicative advantage in bronchioles seen in the first day of infection. Thus the HA mutation may have conferred a survival advantage in the extracellular lung environment. The M1 mutation resulted in improved growth in the lung and cultured cells and was associated with increases in recruitment of macrophages, spread of infection into the alveoli of the lung and interstitial pneumonia. Sequence analysis indicated that the unmapped mutation in the control of FM-MA virulence is either the K482-->R substitution in the PB2 protein or the D538-->G substitution in the PB1 protein. One or other of these mutations results in a growth advantage in infected lung but not in cultured cells as well as a further increased recruitment and infection of macrophages in the lung. Infection with virulent strains of influenza that induced increases in macrophage recruitment caused hypothermia in the mouse. |Animals[MESH] |Chromosome Mapping[MESH] |Flow Cytometry[MESH] |Fluorescent Antibody Technique[MESH] |Hemagglutination Inhibition Tests[MESH] |Hemagglutinin Glycoproteins, Influenza Virus/*genetics[MESH] |Humans[MESH] |Hydrogen-Ion Concentration[MESH] |Hypothermia[MESH] |Influenza A virus/*genetics/growth & development/*pathogenicity[MESH] |Lung/pathology/virology[MESH] |Macrophages/virology[MESH] |Membrane Fusion[MESH] |Mutation[MESH] |RNA-Dependent RNA Polymerase[MESH] |Viral Matrix Proteins/*genetics[MESH] |Viral Proteins/genetics[MESH]Mutations in the hemagglutinin and matrix genes of a virulent influenz(epmc).pdf DeepDyve Pubget Overpricing