tetano
Editor, Senior Moderator
Virology. 2018 Oct 31;526:155-164. doi: 10.1016/j.virol.2018.10.017. [Epub ahead of print]
[h=1]Lack of IFNγ signaling attenuates spread of influenza A virus in vivo and leads to reduced pathogenesis.[/h] Nicol MQ[SUP]1[/SUP], Campbell GM[SUP]1[/SUP], Shaw DJ[SUP]1[/SUP], Dransfield I[SUP]2[/SUP], Ligertwood Y[SUP]1[/SUP], Beard PM[SUP]3[/SUP], Nash AA[SUP]1[/SUP], Dutia BM[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] IFNγ 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 IFNγ receptor (IFNγR[SUP]-/-[/SUP]) 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 IFNγR[SUP]-/-[/SUP] lungs at 2 and 4 dpi. Levels of inflammatory cytokines and chemokines were lower in IFNγR[SUP]-/-[/SUP] mice at 2 dpi and there was less infiltration of monocyte/macrophage lineage cells than in WT mice. There was no difference in CD4[SUP]+[/SUP] and CD8[SUP]+[/SUP] T cells and alveolar macrophages in the bronchoalveolar lavage fluid (BALF) at 2 and 4 dpi but by 4 dpi IFNγR[SUP]-/-[/SUP] mice had significantly higher percentages of neutrophils. Our data strongly suggest that IAV can use the inflammatory response to promote viral spread.
[h=4]KEYWORDS:[/h] Host response; IFNγ; Influenza A virus; Lung inflammation
PMID: 30390564 DOI: 10.1016/j.virol.2018.10.017
[h=1]Lack of IFNγ signaling attenuates spread of influenza A virus in vivo and leads to reduced pathogenesis.[/h] Nicol MQ[SUP]1[/SUP], Campbell GM[SUP]1[/SUP], Shaw DJ[SUP]1[/SUP], Dransfield I[SUP]2[/SUP], Ligertwood Y[SUP]1[/SUP], Beard PM[SUP]3[/SUP], Nash AA[SUP]1[/SUP], Dutia BM[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] IFNγ 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 IFNγ receptor (IFNγR[SUP]-/-[/SUP]) 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 IFNγR[SUP]-/-[/SUP] lungs at 2 and 4 dpi. Levels of inflammatory cytokines and chemokines were lower in IFNγR[SUP]-/-[/SUP] mice at 2 dpi and there was less infiltration of monocyte/macrophage lineage cells than in WT mice. There was no difference in CD4[SUP]+[/SUP] and CD8[SUP]+[/SUP] T cells and alveolar macrophages in the bronchoalveolar lavage fluid (BALF) at 2 and 4 dpi but by 4 dpi IFNγR[SUP]-/-[/SUP] mice had significantly higher percentages of neutrophils. Our data strongly suggest that IAV can use the inflammatory response to promote viral spread.
[h=4]KEYWORDS:[/h] Host response; IFNγ; Influenza A virus; Lung inflammation
PMID: 30390564 DOI: 10.1016/j.virol.2018.10.017