ArticleCell host & microbe2013
Crosstalk between the type 1 interferon and nuclear factor kappa B pathways confers resistance to a lethal virus infection.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
63 citing papers in PubMed, 98 citations in OpenAlex.
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- Orientia tsutsugamushi targets lamin A using Ank effectors and alters chromatin to inhibit NF-κB.Communications biology · 2026Article
- Interferon-α and -β subtypes have temporally distinct roles in containing viral spread and protecting vital organs.Research square · 2026Article
- Leigh Syndrome Pathomechanism Involves Region-Specific Innate Immune Activation in Ndufs4 Knockout Mice.Cellular and molecular neurobiology · 2026Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- The HCMV tegument protein UL88 degrades MyD88 and reduces innate immune activation.Journal of virology · 2025Article
- A combination of major histocompatibility complex (MHC) I overexpression and type I interferon induce mitochondrial dysfunction in human skeletal myoblasts.Journal of cellular physiology · 2025Article
- Orientia tsutsugamushi Ank5 promotes NLRC5 cytoplasmic retention and degradation to inhibit MHC class I expression.Nature communications · 2024Article
- The roles of CD4Molecular therapy. Nucleic acids · 2024Article
- Innate and adaptive immune responses that control lymph-borne viruses in the draining lymph node.Cellular & molecular immunology · 2024Review
- Resistance to African swine fever virus among African domestic pigs appears to be associated with a distinct polymorphic signature in the RelA gene and upregulation of RelA transcription.Virology journal · 2024Article
- The Viral Protein Poly(A) Polymerase Catalytic Subunit Interacts with Guanylate-Binding Proteins 2 to Antagonize the Antiviral Ability of Targeting Ectromelia Virus.International journal of molecular sciences · 2023Article
- Micro- and Macrovascular Effects of Inflammation in Peripheral Artery Disease-Pathophysiology and Translational Therapeutic Approaches.Biomedicines · 2023Review
- Review
- Resistance To Poxvirus Lethality Does Not Require the Necroptosis Proteins RIPK3 or MLKL.Journal of virology · 2023Article
- Role of cytokines in poxvirus host tropism and adaptation.Current opinion in virology · 2022Review
- Interferon partly dictates a divergent transcriptional response in poxvirus-infected and bystander inflammatory monocytes.Cell reports · 2022Article
- Mechanisms regulating transitory suppressive activity of neutrophils in newborns: PMNs-MDSCs in newborns.Journal of leukocyte biology · 2022Article
- Spatiotemporal NF-κB dynamics encodes the position, amplitude, and duration of local immune inputs.Science advances · 2022Article
- Microglial NF-κB drives tau spreading and toxicity in a mouse model of tauopathy.Nature communications · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Nuclear 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.