ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2013
Overcoming NS1-mediated immune antagonism involves both interferon-dependent and independent mechanisms.
Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Meta-analysis of cell- specific transcriptomic data using fuzzy c-means clustering discovers versatile viral responsive genes.BMC bioinformatics · 2017Article
- Comparative analysis of anti-viral transcriptomics reveals novel effects of influenza immune antagonism.BMC immunology · 2015Article
- Virus-like particles activate type I interferon pathways to facilitate post-exposure protection against Ebola virus infection.PloS one · 2015Article
- Mitogen-activated protein kinase-mediated licensing of interferon regulatory factor 3/7 reinforces the cell response to virus.The Journal of biological chemistry · 2014Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
To ensure survival, our immune system must overcome the action of pathogen-encoded immune antagonists, such as influenza A nonstructural protein-1 (NS1). NS1 subverts the host interferon (IFN) response at multiple levels and blocks the induction of IFN-β, a critical antiviral cytokine. This immune antagonism can be overcome in some cases. It has been shown that IFN-β is upregulated by 48 h in the lungs of wild-type C57BL/6 mice infected with influenza A. In contrast, it is shown here that IFNB1 continues to be repressed in IFNAR1(-/-) IL28Rα(-/-) mice, which are deficient in Type-I and III IFN signaling, implying induction of IFNB1 depends on effective IFN signaling. Despite the complete lack of IFN signaling in this system, some IFN stimulated genes (ISGs) were induced following infection with a Flu strain lacking NS1. While the expression of these viral stress-inducible genes (VSIGs) was initially repressed following infection with wild-type Flu, many of these genes became upregulated by 48 h postinfection. These results demonstrate the existence of IFN-independent mechanisms that can overcome NS1-mediated immune antagonism of VSIGs.
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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.