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Crosstalk between the type 1 interferon and nuclear factor kappa B pathways confers resistance to a lethal virus infection

AuthorsRubio, Daniel; Xu, Ren-Huan; Remakus, Sanda; Krouse, Trayce E.; Truckenmiller, Mary Ellen; Thapa, Roshan J.; Balachandran, Siddharth; Alcamí, Antonio ; Norbury, Christopher C.; Sigal, Luis J.
Issue Date2013
CitationCell Host and Microbe 13: 701- 710 (2013)
AbstractNuclear factor kappa B (NF-κB) and type 1 interferon (T1-IFN) signaling are innate immune mechanisms activated upon viral infection. However, the role of NF-κB and its interplay with T1-IFN in antiviral immunity is poorly understood. We show that NF-κB is essential for resistance to ectromelia virus (ECTV), a mouse orthopoxvirus related to the virus causing human smallpox. Additionally, an ECTV mutant lacking an NF-κB inhibitor activates NF-κB more effectively in vivo, resulting in increased proinflammatory molecule transcription in uninfected cells and organs and decreased viral replication. Unexpectedly, NF-κB activation compensates for genetic defects in the T1-IFN pathway, such as a deficiency in the IRF7 transcription factor, resulting in virus control. Thus, overlap between the T1-IFN and NF-κB pathways allows the host to overcome genetic or pathogen-induced deficiencies in T1-IFN and survive an otherwise lethal poxvirus infection. These findings may also explain why some pathogens target both pathways to cause disease. © 2013 Elsevier Inc.
Identifiersdoi: 10.1016/j.chom.2013.04.015
issn: 1931-3128
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