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Genome-wide CRISPR screening identifies TMEM106B as a proviral host factor for SARS-CoV-2.

Author information

Affiliations

  • 1. KU Leuven Department of Microbiology, Immunology and Transplantation, Laboratory of Virology and Chemotherapy, Rega Institute, Leuven, Belgium.
      Authors
    • Baggen J 1
    • Persoons L 1
    • Vanstreels E 1
    • Jansen S 1
    • Van Looveren D 1
    • De Man J 1
    • Jochmans D 1
    • Neyts J 1
    • Dallmeier K 1
    • Thibaut HJ 1
    • Jacquemyn M 1
    • Daelemans D 1
    (12 authors)
  • 2. KU Leuven Department of Human Genetics, Laboratory for Translational Genetics, Leuven, Belgium.
      Authors
    • Boeckx B 2
    • Lambrechts D 2
    (2 authors)
  • 3. KU Leuven Department of Chronic Diseases and Metabolism, Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Leuven, Belgium.
      Authors
    • Geudens V 3
    • Wauters E 3
    • Vanaudenaerde BM 3
    (3 authors)
  • 4. KU Leuven Department of Microbiology, Immunology and Transplantation, Laboratory of Clinical Infectious and Inflammatory Disorders, Leuven, Belgium.
      Authors
    • Wauters J 4
    (1 author)
  • 5. KU Leuven Department of Microbiology, Immunology and Transplantation, Laboratory of Clinical and Epidemiological Virology, Rega Institute, Leuven, Belgium.
      Authors
    • Maes P 5
    (1 author)

ORCIDs linked to this article

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Nature Genetics, 08 Mar 2021, 53(4):435-444
https://doi.org/10.1038/s41588-021-00805-2 PMID: 33686287 

This article is based on a previously available preprint.

Abstract 

The ongoing COVID-19 pandemic has caused a global economic and health crisis. To identify host factors essential for coronavirus infection, we performed genome-wide functional genetic screens with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and human coronavirus 229E. These screens uncovered virus-specific as well as shared host factors, including TMEM41B and PI3K type 3. We discovered that SARS-CoV-2 requires the lysosomal protein TMEM106B to infect human cell lines and primary lung cells. TMEM106B overexpression enhanced SARS-CoV-2 infection as well as pseudovirus infection, suggesting a role in viral entry. Furthermore, single-cell RNA-sequencing of airway cells from patients with COVID-19 demonstrated that TMEM106B expression correlates with SARS-CoV-2 infection. The present study uncovered a collection of coronavirus host factors that may be exploited to develop drugs against SARS-CoV-2 infection or future zoonotic coronavirus outbreaks.

Full text links 

Read article at publisher's site: https://doi.org/10.1038/s41588-021-00805-2

Read article for free, from open access legal sources, via Unpaywall: https://lirias.kuleuven.be/bitstream/123456789/679194/2/Identification%20of%20TMEM106B%20as%20proviral%20host%20factor%20for%20SARS-CoV-2.pdfUnpaywall

References 

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