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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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C6286381!6286381!30390564
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suck abstract from ncbi


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pmid30390564      Virology 2019 ; 526 (ä): 155-64
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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): 155-64 PMID30390564show 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.
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