Evidence map›Paper›PMID 39100693›Full record

ArticleiScience2024

Genome-scale CRISPR-Cas9 screen identifies host factors as potential therapeutic targets for SARS-CoV-2 infection.

Madoka Sakai, Yoshie Masuda, Yusuke Tarumoto, Naoyuki Aihara, Yugo Tsunoda, Michiko Iwata, Yumiko Kamiya, Ryo Komorizono, Takeshi Noda, Kosuke Yusa and 2 more

Abstract read
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Targeting G9a-miScience · 2025
    Article
  8. Review
  9. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    Review
  10. 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

12 authors.

Madoka SakaiLaboratory of RNA Viruses, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Yoshie MasudaLaboratory of Stem Cell Genetics, Department of Biosystems Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Yusuke TarumotoLaboratory of Stem Cell Genetics, Department of Biosystems Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Naoyuki AiharaLaboratory of Veterinary Pathology, Azabu University, Kanagawa 2520206, Japan.
Yugo TsunodaLaboratory of Ultrastructural Virology, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Michiko IwataLaboratory of RNA Viruses, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Yumiko KamiyaLaboratory of Veterinary Pathology, Azabu University, Kanagawa 2520206, Japan.
Ryo KomorizonoLaboratory of RNA Viruses, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Takeshi NodaLaboratory of Ultrastructural Virology, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Kosuke YusaLaboratory of Stem Cell Genetics, Department of Biosystems Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Keizo TomonagaLaboratory of RNA Viruses, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.
Akiko MakinoLaboratory of RNA Viruses, Department of Virus Research, Institute for Life and Medical Sciences, Kyoto University, Kyoto 6068507, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although many host factors important for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been reported, the mechanisms by which the virus interacts with host cells remain elusive. Here, we identified tripartite motif containing (TRIM) 28, TRIM33, euchromatic histone lysine methyltransferase (EHMT) 1, and EHMT2 as proviral factors involved in SARS-CoV-2 infection by CRISPR-Cas9 screening. Our result suggested that TRIM28 may play a role in viral particle formation and that TRIM33, EHMT1, and EHMT2 may be involved in viral transcription and replication. UNC0642, a compound that specifically inhibits the methyltransferase activity of EHMT1/2, strikingly suppressed SARS-CoV-2 growth in cultured cells and reduced disease severity in a hamster infection model. This study suggests that EHMT1/2 may be a therapeutic target for SARS-CoV-2 infection.

Indexed as

Cell biologyMolecular biologyVirology

Identifiers

PMID39100693
PMCPMC11295705

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.