Tissue factor upregulation is associated with SARS-CoV-2 in the lungs of COVID-19 patients.

COVID-19 SARS-CoV-2 fibrin thrombosis tissue factor

Journal

Journal of thrombosis and haemostasis : JTH
ISSN: 1538-7836
Titre abrégé: J Thromb Haemost
Pays: England
ID NLM: 101170508

Informations de publication

Date de publication:
09 2021
Historique:
revised: 02 07 2021
received: 22 12 2020
accepted: 06 07 2021
pubmed: 9 7 2021
medline: 1 9 2021
entrez: 8 7 2021
Statut: ppublish

Résumé

A substantial proportion of patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develop severe/critical coronavirus disease 2019 (COVID-19) characterized by acute respiratory distress syndrome (ARDS) with thrombosis. We tested the hypothesis that SARS-CoV-2--induced upregulation of tissue factor (TF) expression may be responsible for thrombus formation in COVID-19. We compared autopsy lung tissues from 11 patients with COVID-19--associated ARDS with samples from 6 patients with ARDS from other causes (non-COVID-19 ARDS) and 11 normal control lungs. Dual RNA in situ hybridization for SARS-CoV-2 and TF identified sporadic clustered SARS-CoV-2 with prominent co-localization of SARS-CoV-2 and TF RNA. TF expression was 2-fold higher in COVID-19 than in non-COVID-19 ARDS lungs (P = .017) and correlated with the intensity of SARS-CoV-2 staining (R These data suggest that upregulation of TF expression is associated with thrombus formation in COVID-19 lungs and could be a key therapeutic target. Correlation of TF expression with SARS-CoV-2 in lungs of COVID-19 patients also raises the possibility of direct TF induction by the virus.

Sections du résumé

BACKGROUND
A substantial proportion of patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develop severe/critical coronavirus disease 2019 (COVID-19) characterized by acute respiratory distress syndrome (ARDS) with thrombosis.
OBJECTIVES
We tested the hypothesis that SARS-CoV-2--induced upregulation of tissue factor (TF) expression may be responsible for thrombus formation in COVID-19.
METHODS
We compared autopsy lung tissues from 11 patients with COVID-19--associated ARDS with samples from 6 patients with ARDS from other causes (non-COVID-19 ARDS) and 11 normal control lungs.
RESULTS
Dual RNA in situ hybridization for SARS-CoV-2 and TF identified sporadic clustered SARS-CoV-2 with prominent co-localization of SARS-CoV-2 and TF RNA. TF expression was 2-fold higher in COVID-19 than in non-COVID-19 ARDS lungs (P = .017) and correlated with the intensity of SARS-CoV-2 staining (R
CONCLUSIONS
These data suggest that upregulation of TF expression is associated with thrombus formation in COVID-19 lungs and could be a key therapeutic target. Correlation of TF expression with SARS-CoV-2 in lungs of COVID-19 patients also raises the possibility of direct TF induction by the virus.

Identifiants

pubmed: 34236752
doi: 10.1111/jth.15451
pmc: PMC8565501
mid: NIHMS1751126
pii: S1538-7836(22)01901-8
doi:

Substances chimiques

Thromboplastin 9035-58-9

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

2268-2274

Subventions

Organisme : NIGMS NIH HHS
ID : P20 GM103639
Pays : United States
Organisme : NIGMS NIH HHS
ID : GM114731
Pays : United States
Organisme : NIGMS NIH HHS
ID : GM103639
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL148123
Pays : United States
Organisme : NHLBI NIH HHS
ID : HL148123
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA225520
Pays : United States
Organisme : NIGMS NIH HHS
ID : P30 GM114731
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL123605
Pays : United States
Organisme : NHLBI NIH HHS
ID : HL123605
Pays : United States

Informations de copyright

© 2021 International Society on Thrombosis and Haemostasis.

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Auteurs

Sandeep Subrahmanian (S)

Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation (OMRF), Oklahoma City, Oklahoma, USA.

Alain Borczuk (A)

Department of Pathology, Weill Cornell Medical College, New York, New York, USA.

Steven Salvatore (S)

Department of Pathology, Weill Cornell Medical College, New York, New York, USA.

Kar-Ming Fung (KM)

Department of Pathology, University of Oklahoma (HSC), Oklahoma City, Oklahoma, USA.

Joan T Merrill (JT)

Arthritis & Clinical Immunology Research Program, Oklahoma Medical Research Foundation (OMR), Oklahoma City, Oklahoma, USA.

Jeffrey Laurence (J)

Department of Medicine, Weill Cornell Medical College, New York, New York, USA.

Jasimuddin Ahamed (J)

Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation (OMRF), Oklahoma City, Oklahoma, USA.
Department of Pathology, University of Oklahoma (HSC), Oklahoma City, Oklahoma, USA.
Department of Physiology, University of Oklahoma (HSC), Oklahoma City, Oklahoma, USA.

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Classifications MeSH