Visualising SARS-CoV-2 infection of the lung in deceased COVID-19 patients.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Jun 2023
Historique:
received: 23 01 2023
revised: 21 04 2023
accepted: 21 04 2023
medline: 19 6 2023
pubmed: 25 5 2023
entrez: 24 5 2023
Statut: ppublish

Résumé

SARS-CoV-2 is a single-stranded positive-sense RNA virus. Several negative-sense SARS-CoV-2 RNA species, both full-length genomic and subgenomic, are produced transiently during viral replication. Methodologies for rigorously characterising cell tropism and visualising ongoing viral replication at single-cell resolution in histological sections are needed to assess the virological and pathological phenotypes of future SARS-CoV-2 variants. We aimed to provide a robust methodology for examining the human lung, the major target organ of this RNA virus. A prospective cohort study took place at the University Hospitals Leuven in Leuven, Belgium. Lung samples were procured postmortem from 22 patients who died from or with COVID-19. Tissue sections were fluorescently stained with the ultrasensitive single-molecule RNA in situ hybridisation platform of RNAscope combined with immunohistochemistry followed by confocal imaging. We visualised perinuclear RNAscope signal for negative-sense SARS-CoV-2 RNA species in ciliated cells of the bronchiolar epithelium of a patient who died with COVID-19 in the hyperacute phase of the infection, and in ciliated cells of a primary culture of human airway epithelium that had been infected experimentally with SARS-CoV-2. In patients who died between 5 and 13 days after diagnosis of the infection, we detected RNAscope signal for positive-sense but not for negative-sense SARS-CoV-2 RNA species in pneumocytes, macrophages, and among debris in the alveoli. SARS-CoV-2 RNA levels decreased after a disease course of 2-3 weeks, concomitant with a histopathological change from exudative to fibroproliferative diffuse alveolar damage. Taken together, our confocal images illustrate the complexities stemming from traditional approaches in the literature to characterise cell tropism and visualise ongoing viral replication solely by the surrogate parameters of nucleocapsid-immunoreactive signal or in situ hybridisation for positive-sense SARS-CoV-2 RNA species. Confocal imaging of human lung sections stained fluorescently with commercially available RNAscope probes for negative-sense SARS-CoV-2 RNA species enables the visualisation of viral replication at single-cell resolution during the acute phase of the infection in COVID-19. This methodology will be valuable for research on future SARS-CoV-2 variants and other respiratory viruses. Max Planck Society, Coronafonds UZ/KU Leuven, European Society for Organ Transplantation.

Sections du résumé

BACKGROUND BACKGROUND
SARS-CoV-2 is a single-stranded positive-sense RNA virus. Several negative-sense SARS-CoV-2 RNA species, both full-length genomic and subgenomic, are produced transiently during viral replication. Methodologies for rigorously characterising cell tropism and visualising ongoing viral replication at single-cell resolution in histological sections are needed to assess the virological and pathological phenotypes of future SARS-CoV-2 variants. We aimed to provide a robust methodology for examining the human lung, the major target organ of this RNA virus.
METHODS METHODS
A prospective cohort study took place at the University Hospitals Leuven in Leuven, Belgium. Lung samples were procured postmortem from 22 patients who died from or with COVID-19. Tissue sections were fluorescently stained with the ultrasensitive single-molecule RNA in situ hybridisation platform of RNAscope combined with immunohistochemistry followed by confocal imaging.
FINDINGS RESULTS
We visualised perinuclear RNAscope signal for negative-sense SARS-CoV-2 RNA species in ciliated cells of the bronchiolar epithelium of a patient who died with COVID-19 in the hyperacute phase of the infection, and in ciliated cells of a primary culture of human airway epithelium that had been infected experimentally with SARS-CoV-2. In patients who died between 5 and 13 days after diagnosis of the infection, we detected RNAscope signal for positive-sense but not for negative-sense SARS-CoV-2 RNA species in pneumocytes, macrophages, and among debris in the alveoli. SARS-CoV-2 RNA levels decreased after a disease course of 2-3 weeks, concomitant with a histopathological change from exudative to fibroproliferative diffuse alveolar damage. Taken together, our confocal images illustrate the complexities stemming from traditional approaches in the literature to characterise cell tropism and visualise ongoing viral replication solely by the surrogate parameters of nucleocapsid-immunoreactive signal or in situ hybridisation for positive-sense SARS-CoV-2 RNA species.
INTERPRETATION CONCLUSIONS
Confocal imaging of human lung sections stained fluorescently with commercially available RNAscope probes for negative-sense SARS-CoV-2 RNA species enables the visualisation of viral replication at single-cell resolution during the acute phase of the infection in COVID-19. This methodology will be valuable for research on future SARS-CoV-2 variants and other respiratory viruses.
FUNDING BACKGROUND
Max Planck Society, Coronafonds UZ/KU Leuven, European Society for Organ Transplantation.

Identifiants

pubmed: 37224768
pii: S2352-3964(23)00173-1
doi: 10.1016/j.ebiom.2023.104608
pmc: PMC10202122
pii:
doi:

Substances chimiques

RNA, Viral 0
Subgenomic RNA 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

104608

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests SF received support for travel from Pfizer and Gilead. RV received consulting fees from AstraZeneca. JW received consulting and speaker's fees and support for travel from Pfizer, Gilead and MSD.

Auteurs

Jan Van Slambrouck (J)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium; Department of Thoracic Surgery, University Hospitals Leuven, Leuven, Belgium.

Mona Khan (M)

Max Planck Research Unit for Neurogenetics, Frankfurt, Germany.

Erik Verbeken (E)

Department of Imaging and Pathology, KU Leuven, Leuven, Belgium; Department of Pathology, University Hospitals Leuven, Leuven, Belgium.

Sumin Choi (S)

Max Planck Research Unit for Neurogenetics, Frankfurt, Germany.

Vincent Geudens (V)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium.

Cedric Vanluyten (C)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium; Department of Thoracic Surgery, University Hospitals Leuven, Leuven, Belgium.

Simon Feys (S)

Department of Microbiology, Immunology and Transplantation, KU Leuven, Leuven, Belgium; Medical Intensive Care Unit, University Hospitals Leuven, Leuven, Belgium.

Emiel Vanhulle (E)

Department of Microbiology, Immunology and Transplantation, Rega Institute, Laboratory of Virology and Chemotherapy, KU Leuven, Leuven, Belgium.

Elke Wollants (E)

Department of Microbiology, Immunology and Transplantation, Rega Institute, Laboratory of Clinical and Epidemiological Virology, KU Leuven, Leuven, Belgium.

Kurt Vermeire (K)

Department of Microbiology, Immunology and Transplantation, Rega Institute, Laboratory of Virology and Chemotherapy, KU Leuven, Leuven, Belgium.

Charlotte De Fays (C)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium; Pole of Pneumology, ENT, and Dermatology, Institute of Experimental and Clinical Research, Université Catholique de Louvain, Brussels, Belgium.

Lucia Aversa (L)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium.

Janne Kaes (J)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium.

Dirk Van Raemdonck (D)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium; Department of Thoracic Surgery, University Hospitals Leuven, Leuven, Belgium.

Robin Vos (R)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium; Department of Respiratory Diseases, University Hospitals Leuven, Leuven, Belgium.

Bart Vanaudenaerde (B)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium.

Gert De Hertogh (G)

Department of Imaging and Pathology, KU Leuven, Leuven, Belgium; Department of Pathology, University Hospitals Leuven, Leuven, Belgium.

Els Wauters (E)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium; Department of Respiratory Diseases, University Hospitals Leuven, Leuven, Belgium.

Joost Wauters (J)

Department of Microbiology, Immunology and Transplantation, KU Leuven, Leuven, Belgium; Medical Intensive Care Unit, University Hospitals Leuven, Leuven, Belgium.

Laurens J Ceulemans (LJ)

Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), KU Leuven, Leuven, Belgium; Department of Thoracic Surgery, University Hospitals Leuven, Leuven, Belgium.

Peter Mombaerts (P)

Max Planck Research Unit for Neurogenetics, Frankfurt, Germany. Electronic address: peter.mombaerts@gen.mpg.de.

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Classifications MeSH