Key result
Nuclear viral DNA sensors, such as IFI16, play a critical role in detecting pathogenic DNA within the nucleus and initiating immune signaling pathways against nuclear replicating DNA viruses.
This review highlights the paradigm-shifting discovery of nuclear DNA sensors like IFI16, which detect viral DNA within the host nucleus to trigger immune signaling.
Challenges nuclear compartmental dogma of viral DNA sensing; extends innate immunity research to IFI16 and related nuclear sensors.
Detecting pathogenic DNA by intracellular receptors termed "sensors" is critical toward galvanizing host immune responses and eliminating microbial infections. Emerging evidence has challenged the dogma that sensing of viral DNA occurs exclusively in sub-cellular compartments normally devoid of cellular DNA. The interferon-inducible protein IFI16 was shown to bind nuclear viral DNA and initiate immune signaling, culminating in antiviral cytokine secretion. Here, we review the newly characterized nucleus-originating immune signaling pathways, their links to other crucial host defenses, and unique mechanisms by which viruses suppress their functions. We frame these findings in the context of human pathologies associated with nuclear replicating DNA viruses.
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Diner et al. (2015) conducted a review in Viral infections associated with nuclear replicating DNA viruses. Nuclear viral DNA sensors, such as IFI16, play a critical role in detecting pathogenic DNA within the nucleus and initiating immune signaling pathways against nuclear replicating DNA viruses.
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