Lack of IFNγ signaling attenuates spread of influenza A virus in vivo and leads to reduced pathogenesis.
Virology
; 526: 155-164, 2019 01 02.
Article
em En
| MEDLINE
| ID: mdl-30390564
ABSTRACT
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-/-) at a dose which caused severe disease in wild type 129â¯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-/- lungs at 2 and 4 dpi. Levels of inflammatory cytokines and chemokines were lower in IFNγR-/- 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 IFNγR-/- 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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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Vírus da Influenza A
/
Transdução de Sinais
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Receptores de Interferon
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Infecções por Orthomyxoviridae
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Revista:
Virology
Ano de publicação:
2019
Tipo de documento:
Article