Evidence map›Paper›PMID 36851486›Full record

ArticleViruses2023

TMPRSS2 Is Essential for SARS-CoV-2 Beta and Omicron Infection.

Kristin Metzdorf, Henning Jacobsen, Marina C Greweling-Pils, Markus Hoffmann, Tatjana Lüddecke, Felicitas Miller, Lars Melcher, Amy M Kempf, Inga Nehlmeier, Dunja Bruder and 4 more

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

42 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  3. TMPRSS2-mediated coronavirus spike activation and inhibition.Nature structural & molecular biology · 2026
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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 at 3 institutions in 1 country.

Kristin MetzdorfDepartment of Viral Immunology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.ORCID 0000-0002-0862-047X
Henning JacobsenDepartment of Viral Immunology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.ORCID 0000-0002-7831-1330
Marina C Greweling-PilsMouse-Pathology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
Markus HoffmannInfection Biology Unit, German Primate Center, 37077 Göttingen, Germany.ORCID 0000-0003-4603-7696
Tatjana LüddeckeDepartment of Viral Immunology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
Felicitas MillerMouse-Pathology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
Lars MelcherImmune Regulation Group, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
Amy M KempfInfection Biology Unit, German Primate Center, 37077 Göttingen, Germany.
Inga NehlmeierInfection Biology Unit, German Primate Center, 37077 Göttingen, Germany.
Dunja BruderImmune Regulation Group, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
Marek WideraInstitute for Medical Virology, University Hospital, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.ORCID 0000-0001-5417-9307
Sandra CiesekInstitute for Medical Virology, University Hospital, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.ORCID 0000-0002-1802-7565
Stefan PöhlmannInfection Biology Unit, German Primate Center, 37077 Göttingen, Germany.ORCID 0000-0001-6086-9136
Luka Čičin-ŠainDepartment of Viral Immunology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.ORCID 0000-0003-3978-778X
Helmholtz Centre for Infection Research · DEGerman Primate Center · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 pandemic remains a global health threat and novel antiviral strategies are urgently needed. SARS-CoV-2 employs the cellular serine protease TMPRSS2 for entry into lung cells, and TMPRSS2 inhibitors are being developed for COVID-19 therapy. However, the SARS-CoV-2 Omicron variant, which currently dominates the pandemic, prefers the endo/lysosomal cysteine protease cathepsin L over TMPRSS2 for cell entry, raising doubts as to whether TMPRSS2 inhibitors would be suitable for the treatment of patients infected with the Omicron variant. Nevertheless, the contribution of TMPRSS2 to the spread of SARS-CoV-2 in the infected host is largely unclear. In this study, we show that the loss of TMPRSS2 strongly reduced the replication of the Beta variant in the nose, trachea and lung of C57BL/6 mice, and protected the animals from weight loss and disease. The infection of mice with the Omicron variant did not cause disease, as expected, but again, TMPRSS2 was essential for efficient viral spread in the upper and lower respiratory tract. These results identify the key role of TMPRSS2 in SARS-CoV-2 Beta and Omicron infection, and highlight TMPRSS2 as an attractive target for antiviral intervention.

Indexed as

COVID-19SARS-CoV-2AnimalsAntiviral AgentsHumansMiceMice, Inbred C57BLPandemicsSerine EndopeptidasesAntiviral AgentsSerine EndopeptidasesTMPRSS2 protein, humanTMPRSS2 protein, mouseBeta variant (B.1.351)COVID-19in vivomouseOmicron variant (B.1.1.529)SARS-CoV-2transmembrane serine protease TMPRSS2

Identifiers

PMID36851486
PMCPMC9961888
OpenAlexW4317107301

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.