Evidence map›Paper›PMID 41585476›Full record

ArticleiScience2026

FGFR signaling and neddylation facilitate SARS-CoV-2 infection by modulating interferon induction and viral entry, respectively.

Alberto Felix-Lopez, Joaquin Lopez-Orozco, Mohamed Elaish, Nawell Fayad, Zaikun Xu, Tekeleselassie Woldemariam, Bardes B Hassan, Rashmi Panigrahi, Juveriya Qamar Khan, Megha Rohamare and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Alberto Felix-LopezDepartment of Medical Microbiology & Immunology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.
Joaquin Lopez-OrozcoDepartment of Cell Biology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.
Mohamed ElaishDepartment of Cell Biology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.
Nawell FayadDepartment of Cell Biology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.
Zaikun XuDepartment of Cell Biology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.
Tekeleselassie WoldemariamDepartment of Medicine, University of Alberta, Edmonton, AB, Canada.
Bardes B HassanDepartment of Pathology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.
Rashmi PanigrahiDepartment of Biochemistry, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.
Juveriya Qamar KhanDepartment of Biochemistry, Microbiology and Immunology, University of Saskatchewan, Saskatoon, SK, Canada.
Megha RohamareDepartment of Biochemistry, Microbiology and Immunology, University of Saskatchewan, Saskatoon, SK, Canada.
Irv MayersDepartment of Medicine, University of Alberta, Edmonton, AB, Canada.
J N Mark GloverDepartment of Biochemistry, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.
Joyce A WilsonDepartment of Biochemistry, Microbiology and Immunology, University of Saskatchewan, Saskatoon, SK, Canada.
Darryl FalzaranoVaccine and Infectious Disease Organization (VIDO), University of Saskatchewan, Saskatoon, SK, Canada.
Anil KumarDepartment of Biochemistry, Microbiology and Immunology, University of Saskatchewan, Saskatoon, SK, Canada.
Tom C HobmanDepartment of Medical Microbiology & Immunology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, AB, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SARS-CoV-2 is the causative agent of COVID-19, and although vaccines have reduced disease severity, emerging variants remain a significant public health issue. Broadly effective therapeutics, particularly those targeting host pathways essential for coronavirus infection, are still needed. Here, we used a CRISPR knockout screen to identify druggable host factors required for SARS-CoV-2 infection. The screen revealed NAE1 and FGFR1 as key contributors to infection. Inhibitors, either FDA-approved or those in clinical trials, of these pathways reduced replication of both ancestral and contemporary viral variants. Mechanistic studies showed that FGFR1 promotes viral replication through downstream MEK/ERK signaling, while neddylation appears to support viral entry or infectivity rather than replication itself. In a murine model of severe COVID-19, inhibitors of NAE1 and FGFR1 significantly decreased viral load and lung pathology. These findings support the development of host-targeted antiviral strategies.

Indexed as

Biological sciencesMicrobiologyNatural sciencesPharmacologyVirology

Identifiers

PMID41585476
PMCPMC12828524

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.