Visualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
MetadataShow full item record
AbstractThe innate host defense against influenza virus is largely dependent on the type I interferon (IFN) system. However, surprisingly little is known about the cellular source of IFN in the infected lung. To clarify this question, we employed a reporter mouse that contains the firefly luciferase gene in place of the IFN-β-coding region. IFN-β-producing cells were identified either by simultaneous immunostaining of lungs for luciferase and cellular markers or by generating conditional reporter mice that express luciferase exclusively in defined cell types. Two different strains of influenza A virus were employed that either do or do not code for nonstructural protein 1 (NS1), which strongly suppresses innate immune responses of infected cells. We found that epithelial cells and lung macrophages, which represent the prime host cells for influenza viruses, showed vigorous IFN-β responses which, however, were severely reduced and delayed if the infecting virus was able to produce NS1. Interestingly, CD11c(+) cell populations that were either expressing or lacking macrophage markers produced the bulk of IFN-β at 48 h after infection with wild-type influenza A virus. Our results demonstrate that the virus-encoded IFN-antagonistic factor NS1 disarms specifically epithelial cells and lung macrophages, which otherwise would serve as main mediators of the early response against infection by influenza virus.
CitationVisualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1. 2013, 87 (12):6925-30 J. Virol.
AffiliationDepartment of Virology, University of Freiburg, Freiburg, Germany.
JournalJournal of virology
The following license files are associated with this item:
- Alleles A and B of non-structural protein 1 of avian influenza A viruses differentially inhibit beta interferon production in human and mink lung cells.
- Authors: Munir M, Zohari S, Metreveli G, Baule C, Belák S, Berg M
- Issue date: 2011 Sep
- A Conserved Residue, Tyrosine (Y) 84, in H5N1 Influenza A Virus NS1 Regulates IFN Signaling Responses to Enhance Viral Infection.
- Authors: Wang BX, Wei L, Kotra LP, Brown EG, Fish EN
- Issue date: 2017 May 12
- Differences in Type I interferon response in human lung epithelial cells infected by highly pathogenic H5N1 and low pathogenic H11N1 avian influenza viruses.
- Authors: Thube MM, Shil P, Kasbe R, Patil AA, Pawar SD, Mullick J
- Issue date: 2018 Jun
- Interferon-lambda contributes to innate immunity of mice against influenza A virus but not against hepatotropic viruses.
- Authors: Mordstein M, Kochs G, Dumoutier L, Renauld JC, Paludan SR, Klucher K, Staeheli P
- Issue date: 2008 Sep 12
- Cellular transcriptional profiling in influenza A virus-infected lung epithelial cells: the role of the nonstructural NS1 protein in the evasion of the host innate defense and its potential contribution to pandemic influenza.
- Authors: Geiss GK, Salvatore M, Tumpey TM, Carter VS, Wang X, Basler CF, Taubenberger JK, Bumgarner RE, Palese P, Katze MG, García-Sastre A
- Issue date: 2002 Aug 6