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10.1016/j.virol.2018.10.017

http://scihub22266oqcxt.onion/10.1016/j.virol.2018.10.017
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suck abstract from ncbi


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pmid30390564
      Virology 2019 ; 526 (ä): 155-164
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  • Lack of IFN? signaling attenuates spread of influenza A virus in vivo and leads to reduced pathogenesis #MMPMID30390564
  • Nicol MQ ; Campbell GM ; Shaw DJ ; Dransfield I ; Ligertwood Y ; Beard PM ; Nash AA ; Dutia BM
  • Virology 2019[Jan]; 526 (ä): 155-164 PMID30390564 show ga
  • IFN? is a key regulator of inflammatory responses but its role in influenza A virus (IAV) pathogenesis is unclear. Our studies show that infection of mice lacking the IFN? receptor (IFN?R(-/-)) at a dose which caused severe disease in wild type 129?Sv/Ev (WT) mice resulted in milder clinical symptoms and significantly lower lung virus titers by 6 days post-infection (dpi). Viral spread was reduced in IFN?R(-/-) lungs at 2 and 4 dpi. Levels of inflammatory cytokines and chemokines were lower in IFN?R(-/-) mice at 2 dpi and there was less infiltration of monocyte/macrophage lineage cells than in WT mice. There was no difference in CD4(+) and CD8(+) T cells and alveolar macrophages in the bronchoalveolar lavage fluid (BALF) at 2 and 4 dpi but by 4 dpi IFN?R(-/-) mice had significantly higher percentages of neutrophils. Our data strongly suggest that IAV can use the inflammatory response to promote viral spread.
  • |*Signal Transduction/genetics [MESH]
  • |Animals [MESH]
  • |Bronchoalveolar Lavage Fluid/immunology [MESH]
  • |Cytokines/metabolism [MESH]
  • |Influenza A virus/*pathogenicity [MESH]
  • |Interferon gamma Receptor [MESH]
  • |Lung/metabolism/pathology/virology [MESH]
  • |Macrophages/immunology [MESH]
  • |Mice [MESH]
  • |Mice, Transgenic [MESH]
  • |Neutrophils/immunology [MESH]
  • |Orthomyxoviridae Infections/metabolism/*physiopathology/virology [MESH]
  • |Receptors, Interferon/*genetics [MESH]


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