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Bidirectional genome-wide CRISPR screens reveal host factors regulating SARS-CoV-2, MERS-CoV and seasonal HCoVs

Antoine Rebendenne1, Priyanka Roy2, Boris Bonaventure1

  • 1IRIM, CNRS, Montpellier University, Montpellier, France.

Nature Genetics
|July 25, 2022
PubMed

Insights

Multiple cell models reveal new host factors controlling SARS-CoV-2 replication, including AP1G1 and mucins. These findings offer potential therapeutic targets for coronaviruses.

Area of Science:

  • Virology
  • Genomics
  • Cell Biology

Background:

  • CRISPR screens identified host factors for SARS-CoV-2, but results vary by cell type.
  • A meta-analysis showed cell-type specificity, necessitating diverse models for comprehensive host factor identification.

Purpose of the Study:

  • To identify host factors and inhibitors of SARS-CoV-2 replication using multiple cell models and screening approaches.
  • To explore the impact of identified genes on other coronaviruses like MERS-CoV and seasonal HCoVs.
  • To investigate the mechanism of viral entry regulation by identified host factors.

Main Methods:

  • Genome-wide CRISPR knockout (KO) and activation screens were performed in Calu-3 lung and Caco-2 colorectal cells.
  • Secondary screens were conducted in four additional human cell lines.
  • Meta-analysis of existing CRISPR screen data was performed.

Main Results:

  • Identified host-dependency factors (e.g., AP1G1, ATP8B1) and inhibitors (e.g., mucins) of SARS-CoV-2.
  • Discovered that some identified genes also affect MERS-CoV and seasonal human coronavirus replication.
  • Found that most genes impact viral entry, with AP1G1 potentially regulating TMPRSS2 activity.

Conclusions:

  • Utilizing multiple cell models and screening methods is crucial for a complete understanding of SARS-CoV-2 host-dependency.
  • The study provides a list of novel host factors and inhibitors that could be targeted for therapeutic interventions against coronaviruses.
  • AP1G1's role in regulating TMPRSS2 activity highlights a specific mechanism for viral entry modulation.

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