Key result
Nlrp6 deficiency in mice orally infected with enteric viruses resulted in increased mortality, viremia, and gastrointestinal viral loads compared with controls.
Why the study?
Does Nlrp6 regulate intestinal antiviral innate immunity in mice infected with enteric viruses?
Does Nlrp6 regulate intestinal antiviral innate immunity in mice infected with enteric viruses?
Nlrp6 functions with Dhx15 as a viral RNA sensor to induce interferon-stimulated genes, playing a crucial role in intestinal antiviral innate immunity.
Answers are grounded in this paper and cite their sources.
Nlrp6 supports intestinal antiviral defense in mice; leaves open relevance to human enteric infections or therapy.
The nucleotide-binding oligomerization domain-like receptor (Nlrp) 6 maintains gut microbiota homeostasis and regulates antibacterial immunity. We now report a role for Nlrp6 in the control of enteric virus infection. Nlrp6(-/-) and control mice systemically challenged with encephalomyocarditis virus had similar mortality; however, the gastrointestinal tract of Nlrp6(-/-) mice exhibited increased viral loads. Nlrp6(-/-) mice orally infected with encephalomyocarditis virus had increased mortality and viremia compared with controls. Similar results were observed with murine norovirus 1. Nlrp6 bound viral RNA via the RNA helicase Dhx15 and interacted with mitochondrial antiviral signaling protein to induce type I/III interferons (IFNs) and IFN-stimulated genes (ISGs). These data demonstrate that Nlrp6 functions with Dhx15 as a viral RNA sensor to induce ISGs, and this effect is especially important in the intestinal tract.
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Wang et al. (2015) studied Enteric virus infection. Nlrp6 deficiency vs. Control mice was evaluated on Mortality, viral loads, and viremia. Nlrp6 deficiency in mice orally infected with enteric viruses resulted in increased mortality, viremia, and gastrointestinal viral loads compared with controls.
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