ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
Type I Interferons Act Directly on Nociceptors to Produce Pain Sensitization: Implications for Viral Infection-Induced Pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 99 citations in OpenAlex.
- Microglial MARCO facilitates Varicella zoster virus uptake and triggers TLR2-mediated neuroinflammation.Journal of biomedical science · 2026Article
- Live cell imaging reveals paclitaxel-induced lysosome motility and function disruption in DRG neurons.bioRxiv : the preprint server for biology · 2026Article
- Neuroimmune interferon signals sustain arthritis pain.Nature neuroscience · 2026Article
- Persistent interferon signaling causes sensory neuron plasticity and pain before and during arthritis.Nature neuroscience · 2026Article
- Nociceptor neurons shape antiviral immunity.Journal of neuroinflammation · 2026Review
- IRF7 Modulates Inflammatory Pain Through Upregulating IFNβ in Mice Trigeminal Ganglion.Inflammation · 2026Article
- Article
- Progressive neurodegeneration in human dorsal root ganglion from diabetes to painful neuropathy.bioRxiv : the preprint server for biology · 2026Article
- Nociplastic pain: the prominent role of non-neuronal cells in central and peripheral sensitization.Frontiers in immunology · 2026Review
- Blood transcriptomic immune signatures in herpes zoster and postherpetic neuralgia: parallel cohort analyses of IFN-related pathway patterns.Frontiers in cellular and infection microbiology · 2026Article
- A molecular map of the human spinal dorsal and ventral horn defines arrangement of neuronal types and glial sex differences.bioRxiv : the preprint server for biology · 2025Article
- Type I IFNs enhance human dorsal root ganglion nociceptor excitability and induce TRPV1 sensitization.JCI insight · 2025Article
- Peripheral nerve-targeting and pain-promoting transcriptomic signatures in early Guillain-Barré syndrome.bioRxiv : the preprint server for biology · 2025Article
- Review
- Rheumatoid arthritis synovial fluid induces JAK-dependent intracellular activation of human sensory neurons.JCI insight · 2025Article
- Decoding mechanisms and protein markers in lung-brain axis.Respiratory research · 2025Review
- Innate immune pathway activated mesenchymal stromal cells improve function and histologic outcomes in a rodent osteoarthritis model.Frontiers in bioengineering and biotechnology · 2025Article
- Small fiber neuropathy associated with COVID-19 infection and vaccination: A prospective case-control study.European journal of neurology · 2025Article
- Article
- An interdisciplinary perspective on peripheral drivers of pain in rheumatoid arthritis.Nature reviews. Rheumatology · 2024Review
8 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
9 authors at 2 institutions in 2 countries.
Funding
Abstract
One of the first signs of viral infection is body-wide aches and pain. Although this type of pain usually subsides, at the extreme, viral infections can induce painful neuropathies that can last for decades. Neither of these types of pain sensitization is well understood. A key part of the response to viral infection is production of interferons (IFNs), which then activate their specific receptors (IFNRs) resulting in downstream activation of cellular signaling and a variety of physiological responses. We sought to understand how type I IFNs (IFN-α and IFN-β) might act directly on nociceptors in the dorsal root ganglion (DRG) to cause pain sensitization. We demonstrate that type I IFNRs are expressed in small/medium DRG neurons and that their activation produces neuronal hyper-excitability and mechanical pain in mice. Type I IFNs stimulate JAK/STAT signaling in DRG neurons but this does not apparently result in PKR-eIF2α activation that normally induces an anti-viral response by limiting mRNA translation. Rather, type I IFNs stimulate MNK-mediated eIF4E phosphorylation in DRG neurons to promote pain hypersensitivity. Endogenous release of type I IFNs with the double-stranded RNA mimetic poly(I:C) likewise produces pain hypersensitivity that is blunted in mice lacking MNK-eIF4E signaling. Our findings reveal mechanisms through which type I IFNs cause nociceptor sensitization with implications for understanding how viral infections promote pain and can lead to neuropathies.
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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.