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In Vivo Conditions Enable IFNAR-Independent Type I Interferon Production by Peritoneal CD11b+ Cells upon Thogoto Virus Infection.

Kochs, Georg
; 
Anzaghe, Martina
; 
Kronhart, Stefanie
; 
Wagner, Valentina
; 
Gogesch, Patricia
; 
Scheu, Stefanie
; ; 
Waibler, Zoe
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Issue Date
2016-10-15
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Abstract
Type I interferons (IFNs) crucially contribute to host survival upon viral infections. Robust expression of type I IFNs (IFN-α/β) and induction of an antiviral state critically depend on amplification of the IFN signal via the type I IFN receptor (IFNAR). A small amount of type I IFN produced early upon virus infection binds the IFNAR and activates a self-enhancing positive feedback loop, resulting in induction of large, protective amounts of IFN-α. Unexpectedly, we found robust, systemic IFN-α expression upon infection of IFNAR knockout mice with the orthomyxovirus Thogoto virus (THOV). The IFNAR-independent IFN-α production required in vivo conditions and was not achieved during in vitro infection. Using replication-incompetent THOV-derived virus-like particles, we demonstrate that IFNAR-independent type I IFN induction depends on viral polymerase activity but is largely independent of viral replication. To discover the cell type responsible for this effect, we used type I IFN reporter mice and identified CD11b(+) F4/80(+) myeloid cells within the peritoneal cavity of infected animals as the main source of IFNAR-independent type I IFN, corresponding to the particular tropism of THOV for this cell type.
Citation
In Vivo Conditions Enable IFNAR-Independent Type I Interferon Production by Peritoneal CD11b+ Cells upon Thogoto Virus Infection. 2016, 90 (20):9330-7 J. Virol.
Affiliation
Medizinische Hochschule Hannover: Hannover, Niedersachsen, Germany.
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Journal
Journal of virology
URI
http://hdl.handle.net/10033/620545
DOI
10.1128/JVI.00744-16
PubMed ID
27512061
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Article
Language
en
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1098-5514
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publications of the research group molecular Immunology (MOLI)