Evidence map›Paper›PMID 33143316›Full record

ArticleCells2020

Aprotinin Inhibits SARS-CoV-2 Replication.

Denisa Bojkova, Marco Bechtel, Katie-May McLaughlin, Jake E McGreig, Kevin Klann, Carla Bellinghausen, Gernot Rohde, Danny Jonigk, Peter Braubach, Sandra Ciesek and 4 more

Abstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing 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

51 citing papers in PubMed.

  1. Trial
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  10. Article
  11. Aprotinin-Drug against Respiratory Diseases.International journal of molecular sciences · 2023
    Review
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  13. 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

14 authors.

Denisa BojkovaInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.
Marco BechtelInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.
Katie-May McLaughlinSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.
Jake E McGreigSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.ORCID 0000-0002-3068-5624
Kevin KlannFaculty of Medicine, Institute of Biochemistry II, Goethe University, 60590 Frankfurt am Main, Germany.ORCID 0000-0003-2276-8128
Carla BellinghausenDepartment of Respiratory Medicine and Allergology, University Hospital, Goethe University, 60590 Frankfurt am Main, Germany.ORCID 0000-0001-8025-2846
Gernot RohdeDepartment of Respiratory Medicine and Allergology, University Hospital, Goethe University, 60590 Frankfurt am Main, Germany.ORCID 0000-0002-5193-7755
Danny JonigkInstitute of Pathology, Hannover Medical School (MHH), 30625 Hannover, Germany.
Peter BraubachInstitute of Pathology, Hannover Medical School (MHH), 30625 Hannover, Germany.
Sandra CiesekInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.ORCID 0000-0002-1802-7565
Christian MünchFaculty of Medicine, Institute of Biochemistry II, Goethe University, 60590 Frankfurt am Main, Germany.ORCID 0000-0003-3832-090X
Mark N WassSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.ORCID 0000-0001-5428-6479
Martin MichaelisSchool of Biosciences, University of Kent, Canterbury CT2 7NJ, UK.ORCID 0000-0002-5710-5888
Jindrich CinatlInstitute for Medical Virology, University Hospital, Goethe University, 60596 Frankfurt am Main, Germany.

Funding

Frankfurter Stiftung für krebskranke Kinder n/aHilfe für krebskranke Kinder Frankfurt e.V. n/a
6 · The paper itself

Abstract

Severe acute respiratory syndrome virus 2 (SARS-CoV-2) is the cause of the current coronavirus disease 19 (COVID-19) pandemic. Protease inhibitors are under consideration as virus entry inhibitors that prevent the cleavage of the coronavirus spike (S) protein by cellular proteases. Herein, we showed that the protease inhibitor aprotinin (but not the protease inhibitor SERPINA1/alpha-1 antitrypsin) inhibited SARS-CoV-2 replication in therapeutically achievable concentrations. An analysis of proteomics and translatome data indicated that SARS-CoV-2 replication is associated with a downregulation of host cell protease inhibitors. Hence, aprotinin may compensate for downregulated host cell proteases during later virus replication cycles. Aprotinin displayed anti-SARS-CoV-2 activity in different cell types (Caco2, Calu-3, and primary bronchial epithelial cell air-liquid interface cultures) and against four virus isolates. In conclusion, therapeutic aprotinin concentrations exert anti-SARS-CoV-2 activity. An approved aprotinin aerosol may have potential for the early local control of SARS-CoV-2 replication and the prevention of COVID-19 progression to a severe, systemic disease.

Indexed as

COVID-19 Drug TreatmentAnimalsAntiviral AgentsAprotininCaco-2 CellsChlorocebus aethiopsCOVID-19Epithelial CellsHumansPandemicsSARS-CoV-2Serine Proteinase InhibitorsVero CellsVirus ReplicationAntiviral AgentsAprotininSerine Proteinase Inhibitors2019-nCoVantiviralaprotininCOVID-19drug discoverysevere acute respiratory syndrome coronavirussevere acute respiratory syndrome coronavirus 2

Identifiers

PMID33143316
PMCPMC7692688

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.