Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Zhenlan YaoDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0001-6588-0633
Pablo A AlvarezDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0002-0079-3392
Carolina ChavezDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Yennifer DelgadoDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0002-7582-8545
Prashant KaushalDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.
David W BuchholzDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0001-8874-6648
David AustinDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.ORCID 0000-0003-0003-9485
Qian LiDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Yanying YuCenter for Infection Biology, School of Basic Medical Sciences, Tsinghua University, Beijing, China.
Anne K ZaissDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.ORCID 0009-0003-7003-4724
Vaithilingaraja ArumugaswamiDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.ORCID 0000-0002-6872-5118
Qiang DingCenter for Infection Biology, School of Basic Medical Sciences, Tsinghua University, Beijing, China.
Jeffrey J HsuDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0002-9971-5916
Robert DamoiseauxDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.ORCID 0000-0002-7611-7534
Hector C AguilarDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0001-6879-8360
Mehdi BouhaddouDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0002-9526-1427
Alexander HoffmannDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0002-5607-3845
Melody M H LiDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.ORCID 0000-0002-6905-7940
Funding
Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ZACK, JEROME A. · 1991 to 2018
$39.9M
MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
Mechanisms of Nipah virus fusion and entryR01AI109022 · NIAID · WASHINGTON STATE UNIVERSITY · PI AGUILAR-CARRENO, HECTOR · 2014 to 2024
$4.3M
Characterizing functional states of macrophages via their stimulus-responsesR01AI173214 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Alexander Hoffmann · 2023 to 2026
$2.8M
Functional analysis of host and viral determinants for ZAP inhibitionR01AI158704 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LI, MELODY · 2021 to 2025
$1.9M
The IRF regulatory network in innate immune training of macrophagesR01AI185026 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Alexander Hoffmann · 2025 to 2026
$1.3M
Unraveling alphavirus neuroinvasion: Molecular insights from a stem cell based blood-brain barrier modelF31AI179235 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ALVAREZ, PABLO · 2024 to 2025
A substantial proportion of hospitalized COVID-19 patients require ICU admission, often associated with an imbalance between antiviral responses and inflammatory signaling leading to uncontrolled cytokine secretion. The SARS-CoV-2 nucleocapsid (N) protein is a known immune antagonist, but its role in macrophage-driven cytokine storms is unclear. We demonstrate that N functions in a stimulus-specific manner, specifically amplifying extracellular and dampening intracellular RNA sensing. Moreover, we show that this is a conserved feature of pathogenic betacoronaviruses through distinct mechanisms. Our interaction networks with SARS-CoV-2 variant N proteins suggest that the Delta variant N drives inflammation through interactions with several proteins, most notably, cGAS. Profiling of secreted cytokines revealed that N disrupts the secretome in a variant-specific manner. Most notably, we found that supernatants from the Delta variant N-expressing macrophages dramatically disrupt heart endothelial barriers, implicating N in COVID-19-associated cardiac complications. Our findings highlight N-mediated immune imbalance as a driver of severe COVID-19 and identify N as a promising therapeutic target to mitigate hyperinflammation.
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.
SARS-CoV-2 nucleocapsid induces hyperinflammation and vascular leakage through the Toll-like receptor signaling axis in macrophages. · full record | OpenQuestion