Evidence map›Paper›PMID 35455942›Full record

ArticleCells2022

SMYD2 Inhibition Downregulates TMPRSS2 and Decreases SARS-CoV-2 Infection in Human Intestinal and Airway Epithelial Cells.

Yu-Qiang Yu, Alexandra Herrmann, Veronika Thonn, Arne Cordsmeier, Markus F Neurath, Armin Ensser, Christoph Becker

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Frontiers in cellular and infection microbiology · 2022
    Review
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

7 authors at 2 institutions in 2 countries.

Yu-Qiang YuDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.ORCID 0000-0002-4847-8877
Alexandra HerrmannInstitute of Clinical and Molecular Virology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.
Veronika ThonnDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.
Arne CordsmeierInstitute of Clinical and Molecular Virology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.
Markus F NeurathDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.
Armin EnsserInstitute of Clinical and Molecular Virology, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.ORCID 0000-0001-8873-3863
Christoph BeckerDepartment of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 91052 Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEDuke University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 pandemic caused by SARS-CoV-2 has lasted for more than two years. Despite the presence of very effective vaccines, the number of virus variants that escape neutralizing antibodies is growing. Thus, there is still a need for effective antiviral treatments that target virus replication independently of the circulating variant. Here, we show for the first time that deficiency or pharmacological inhibition of the cellular lysine-methyltransferase SMYD2 decreases TMPRSS2 expression on both mRNA and protein levels. SARS-CoV-2 uses TMPRSS2 for priming its spike protein to infect target cells. Treatment of cultured cells with the SMYD2 inhibitors AZ505 or BAY598 significantly inhibited viral replication. In contrast, treatment of Vero E6 cells, which do not express detectable amounts of TMPRSS2, had no effect on SARS-CoV-2 infection. Moreover, by generating a recombinant reporter virus that expresses the spike protein of the Delta variant of SARS-CoV-2, we demonstrate that BAY598 exhibits similar antiviral activity against this variant of concern. In summary, SMYD2 inhibition downregulates TMPRSS2 and blocks viral replication. Targeting cellular SMYD2 represents a promising tool to curtail SARS-CoV-2 infection.

Indexed as

COVID-19Epithelial CellsHistone-Lysine N-MethyltransferaseSerine EndopeptidasesAntiviral AgentsHumansSARS-CoV-2Spike Glycoprotein, CoronavirusVirus InternalizationAntiviral AgentsHistone-Lysine N-MethyltransferaseSerine EndopeptidasesSMYD2 protein, humanSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2TMPRSS2 protein, humanantiviral treatmentAZ505BAY598COVID-19SARS-CoV-2SMYD2TMPRSS2

Identifiers

PMID35455942
PMCPMC9033063
OpenAlexW4224250761

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.