Evidence map›Paper›PMID 37821447›Full record

ArticleNature communications2023

SARS-CoV-2 infection of human lung epithelial cells induces TMPRSS-mediated acute fibrin deposition.

Rachel Erickson, Chang Huang, Cameron Allen, Joanna Ireland, Gwynne Roth, Zhongcheng Zou, Jinghua Lu, Bernard A P Lafont, Nicole L Garza, Beniah Brumbaugh and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
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

14 citing papers in PubMed, 12 citations in OpenAlex.

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  12. Frontiers in pharmacology · 2025
    Article
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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

18 authors at 2 institutions in 1 country.

Rachel Erickson *Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.ORCID 0000-0001-8857-4583
Chang Huang *Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.ORCID 0000-0002-9836-8166
Cameron Allen *Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.ORCID 0000-0002-6285-8841
Joanna IrelandLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.
Gwynne RothLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.ORCID 0000-0002-2579-2812
Zhongcheng ZouLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.
Jinghua LuLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.
Bernard A P LafontSARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.ORCID 0000-0003-2140-6205
Nicole L GarzaSARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Beniah BrumbaughResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT, 59840, USA.
Ming ZhaoResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.
Motoshi SuzukiResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.
Lisa OlanoResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.ORCID 0000-0003-4862-3170
Joseph BrzostowskiLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA.ORCID 0000-0003-0257-3905
Elizabeth R FischerResearch Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT, 59840, USA.
Homer L TwiggDivision of Pulmonary, Critical Care, Sleep, and Occupational Medicine, Indiana University Medical Center, 1120 West Michigan Street, CL 260A, Indianapolis, IN, 46202, USA.
Reed F JohnsonSARS-CoV-2 Virology Core, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Peter D SunLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 5625 Fishers Ln, Rockville, MD, 20852, USA. psun@nih.gov.ORCID 0000-0003-0475-1891
National Institutes of Health · USUniversity Medical Center · US

Funding

Inhibition of COVID-19 associated acute fibrin deposition in lungZIAAI001263 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SUN, PETER D. · 2020 to 2025
$1.8M
Intramural NIH HHS ZIA AI001263
6 · The paper itself

Abstract

Severe COVID-associated lung injury is a major confounding factor of hospitalizations and death with no effective treatments. Here, we describe a non-classical fibrin clotting mechanism mediated by SARS-CoV-2 infected primary lung but not other susceptible epithelial cells. This infection-induced fibrin formation is observed in all variants of SARS-CoV-2 infections, and requires thrombin but is independent of tissue factor and other classical plasma coagulation factors. While prothrombin and fibrinogen levels are elevated in acute COVID BALF samples, fibrin clotting occurs only with the presence of viral infected but not uninfected lung epithelial cells. We suggest a viral-induced coagulation mechanism, in which prothrombin is activated by infection-induced transmembrane serine proteases, such as ST14 and TMPRSS11D, on NHBE cells. Our finding reveals the inefficiency of current plasma targeted anticoagulation therapy and suggests the need to develop a viral-induced ARDS animal model for treating respiratory airways with thrombin inhibitors.

Indexed as

COVID-19AnimalsEpithelial CellsFibrinHumansLungProthrombinSARS-CoV-2ThrombinFibrinProthrombinThrombin

Identifiers

PMID37821447
PMCPMC10567911
OpenAlexW4387526183

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.