Abstract:
:Interferon gamma (IFNγ) has complex immunomodulatory and antiviral properties. While IFNγ is detected in the airways in response to infection with the pneumovirus pathogen, pneumonia virus of mice (PVM; Family Paramyxoviridae), its role in promoting disease has not been fully explored. Here, we evaluate PVM infection in IFNγ(-/-) mice. Although the IFNγ gene-deletion has no impact on weight loss, survival or virus kinetics, expression of IFNβ, IFNλ2/3 and IFN-stimulated 2-5' oligoadenylate synthetases was significantly diminished compared to wild-type counterparts. Furthermore, PVM infection in IFNγ(-/-) mice promoted prominent inflammation, including eosinophil and neutrophil infiltration into the airways and lung parenchyma, observed several days after peak virus titer. Potential mechanisms include over-production of chemoattractant and eosinophil-active cytokines (CXCL1, CCL11, CCL3 and IL5) in PVM-infected IFNγ(-/-) mice; likewise, IFNγ actively antagonized IL5-dependent eosinophil survival ex vivo. Our results may have clinical implications for pneumovirus infection in individuals with IFNγ signaling defects.
journal_name
Virologyjournal_title
Virologyauthors
Glineur SF,Bowen AB,Percopo CM,Garcia-Crespo KE,Dyer KD,Ochkur SI,Lee NA,Lee JJ,Domachowske JB,Rosenberg HFdoi
10.1016/j.virol.2014.07.039subject
Has Abstractpub_date
2014-11-01 00:00:00pages
140-149eissn
0042-6822issn
1096-0341pii
S0042-6822(14)00354-7journal_volume
468-470pub_type
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