Biodistribution and serologic response in SARS-CoV-2 induced ARDS: A cohort study.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2020
Historique:
received: 01 09 2020
accepted: 12 11 2020
entrez: 24 11 2020
pubmed: 25 11 2020
medline: 15 12 2020
Statut: epublish

Résumé

The viral load and tissue distribution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain important questions. The current study investigated SARS-CoV-2 viral load, biodistribution and anti-SARS-CoV-2 antibody formation in patients suffering from severe corona virus disease 2019 (COVID-19) induced acute respiratory distress syndrome (ARDS). This is a retrospective single-center study in 23 patients with COVID-19-induced ARDS. Data were collected within routine intensive care. SARS-CoV-2 viral load was assessed via reverse transcription quantitative polymerase chain reaction (RT-qPCR). Overall, 478 virology samples were taken. Anti-SARS-CoV-2-Spike-receptor binding domain (RBD) antibody detection of blood samples was performed with an enzyme-linked immunosorbent assay. Most patients (91%) suffered from severe ARDS during ICU treatment with a 30-day mortality of 30%. None of the patients received antiviral treatment. Tracheal aspirates tested positive for SARS-CoV-2 in 100% of the cases, oropharyngeal swabs only in 77%. Blood samples were positive in 26% of the patients. No difference of viral load was found in tracheal or blood samples with regard to 30-day survival or disease severity. SARS-CoV-2 was never found in dialysate. Serologic testing revealed significantly lower concentrations of SARS-CoV-2 neutralizing IgM and IgA antibodies in survivors compared to non-survivors (p = 0.009). COVID-19 induced ARDS is accompanied by a high viral load of SARS-CoV-2 in tracheal aspirates, which remained detectable in the majority throughout intensive care treatment. Remarkably, SARS-CoV-2 RNA was never detected in dialysate even in patients with RNAemia. Viral load or the buildup of neutralizing antibodies was not associated with 30-day survival or disease severity.

Sections du résumé

BACKGROUND
The viral load and tissue distribution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain important questions. The current study investigated SARS-CoV-2 viral load, biodistribution and anti-SARS-CoV-2 antibody formation in patients suffering from severe corona virus disease 2019 (COVID-19) induced acute respiratory distress syndrome (ARDS).
METHODS
This is a retrospective single-center study in 23 patients with COVID-19-induced ARDS. Data were collected within routine intensive care. SARS-CoV-2 viral load was assessed via reverse transcription quantitative polymerase chain reaction (RT-qPCR). Overall, 478 virology samples were taken. Anti-SARS-CoV-2-Spike-receptor binding domain (RBD) antibody detection of blood samples was performed with an enzyme-linked immunosorbent assay.
RESULTS
Most patients (91%) suffered from severe ARDS during ICU treatment with a 30-day mortality of 30%. None of the patients received antiviral treatment. Tracheal aspirates tested positive for SARS-CoV-2 in 100% of the cases, oropharyngeal swabs only in 77%. Blood samples were positive in 26% of the patients. No difference of viral load was found in tracheal or blood samples with regard to 30-day survival or disease severity. SARS-CoV-2 was never found in dialysate. Serologic testing revealed significantly lower concentrations of SARS-CoV-2 neutralizing IgM and IgA antibodies in survivors compared to non-survivors (p = 0.009).
CONCLUSIONS
COVID-19 induced ARDS is accompanied by a high viral load of SARS-CoV-2 in tracheal aspirates, which remained detectable in the majority throughout intensive care treatment. Remarkably, SARS-CoV-2 RNA was never detected in dialysate even in patients with RNAemia. Viral load or the buildup of neutralizing antibodies was not associated with 30-day survival or disease severity.

Identifiants

pubmed: 33232382
doi: 10.1371/journal.pone.0242917
pii: PONE-D-20-27460
pmc: PMC7685466
doi:

Substances chimiques

Antibodies, Neutralizing 0
Antibodies, Viral 0
Immunoglobulin A 0
Immunoglobulin G 0
Immunoglobulin M 0
RNA, Viral 0
Spike Glycoprotein, Coronavirus 0
spike protein, SARS-CoV-2 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0242917

Déclaration de conflit d'intérêts

T. Schlesinger, B. Weißbrich, F. Wedekink, Q. Notz, J. Herrmann, M. Krone, M. Sitter, B. Schmid, L. Dölken, P. Kranke, C. Lotz have nothing to disclose. M. Kredel reports personal fees from Pfizer, outside the submitted work. J. Wischhusen reports personal fees from CatalYm GmbH, outside the submitted work. P. Meybohm reports grants from B. Braun Melsungen, grants from CSL Behring, grants from Fresenius Kabi, grants from Vifor Pharma, outside the submitted work. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

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Auteurs

Tobias Schlesinger (T)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Benedikt Weißbrich (B)

Institute for Virology and Immunobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.

Florian Wedekink (F)

Institute of Obstetrics and Gynecology, University Hospital of Wuerzburg, Wuerzburg, Germany.

Quirin Notz (Q)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Johannes Herrmann (J)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Manuel Krone (M)

Institute for Hygiene and Microbiology, University of Wuerzburg, Wuerzburg, Germany.

Magdalena Sitter (M)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Benedikt Schmid (B)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Markus Kredel (M)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Jan Stumpner (J)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Lars Dölken (L)

Institute for Virology and Immunobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.
Helmholtz Institute for RNA-based Infection Research (HIRI), Helmholtz-Center for Infection Research (HZI), Wuerzburg, Germany.

Jörg Wischhusen (J)

Institute of Obstetrics and Gynecology, University Hospital of Wuerzburg, Wuerzburg, Germany.

Peter Kranke (P)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Patrick Meybohm (P)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

Christopher Lotz (C)

Department of Anesthesiology and Critical Care, University Hospital of Wuerzburg, Wuerzburg, Germany.

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Classifications MeSH