ArticleNature communications2024
Disparate macrophage responses are linked to infection outcome of Hantan virus in humans or rodents.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
The trial behind it
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Cardiopulmonary Failure in Hantavirus Disease: Mechanisms, Recognition, and ECMO-Based Management.Viruses · 2026Review
- Omics Approaches in Hantavirus Research: Current Advances, Challenges, and Future Perspectives.Biotech (Basel (Switzerland)) · 2026Review
- Going wild: prioritizing experimental models of rodent-borne viruses to decode zoonotic spillover and pandemic risk.Journal of virology · 2026Review
- Potential Effects of Bee Products Against Hantavirus Infection: Potential Mechanisms of Action and Future Directions.Life (Basel, Switzerland) · 2026Review
- Clinical Value the Neutrophil CD64 Index in Predicting the Severity of Hemorrhagic Fever With Renal Syndrome.Immunity, inflammation and disease · 2026Article
- Effect ofMicroorganisms · 2026Article
- The role of immune cells in Hantaan-induced hemorrhagic fever with renal syndrome.Frontiers in immunology · 2026Review
- Temporal dynamics of macrophage activation duringVirulence · 2025Article
- Unique transcriptomic responses of rat and human alveolar macrophages in an in vitro model of overload with TiOParticle and fibre toxicology · 2025Article
- Canonical and noncanonical NOTCH signaling in the nongenetic resistance of cancer: distinct and concerted control.Frontiers of medicine · 2025Review
- Visualizing early allograft rejection: an M1 macrophage-specific GLUT1 probe predicts TCMR onset in renal transplantation.Frontiers in immunology · 2025Article
- Isolation and characterization of genetic variants of Orthohantavirus hantanense from clinical cases of HFRS in Jiangxi Province, China.PLoS neglected tropical diseases · 2024Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
Abstract
Hantaan virus (HTNV) is asymptomatically carried by rodents, yet causes lethal hemorrhagic fever with renal syndrome in humans, the underlying mechanisms of which remain to be elucidated. Here, we show that differential macrophage responses may determine disparate infection outcomes. In mice, late-phase inactivation of inflammatory macrophage prevents cytokine storm syndrome that usually occurs in HTNV-infected patients. This is attained by elaborate crosstalk between Notch and NF-κB pathways. Mechanistically, Notch receptors activated by HTNV enhance NF-κB signaling by recruiting IKKβ and p65, promoting inflammatory macrophage polarization in both species. However, in mice rather than humans, Notch-mediated inflammation is timely restrained by a series of murine-specific long noncoding RNAs transcribed by the Notch pathway in a negative feedback manner. Among them, the lnc-ip65 detaches p65 from the Notch receptor and inhibits p65 phosphorylation, rewiring macrophages from the pro-inflammation to the pro-resolution phenotype. Genetic ablation of lnc-ip65 leads to destructive HTNV infection in mice. Thus, our findings reveal an immune-braking function of murine noncoding RNAs, offering a special therapeutic strategy for HTNV infection.
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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 Socratic graph.