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Bidirectional genome-wide CRISPR screens reveal host factors regulating SARS-CoV-2, MERS-CoV and seasonal HCoVs. 2022
Antoine Rebendenne, and
Priyanka Roy, and
Boris Bonaventure, and
Ana Luiza Chaves Valadão, and
Lowiese Desmarets, and
Mary Arnaud-Arnould, and
Yves Rouillé, and
Marine Tauziet, and
Donatella Giovannini, and
Jawida Touhami, and
Yenarae Lee, and
Peter DeWeirdt, and
Mudra Hegde, and
Serge Urbach, and
Khadija El Koulali, and
Francisco Garcia de Gracia, and
Joe McKellar, and
Jean Dubuisson, and
Mélanie Wencker, and
Sandrine Belouzard, and
Olivier Moncorgé, and
John G Doench, and
Caroline Goujon
IRIM, CNRS, Montpellier University, Montpellier, France.
CRISPR knockout (KO) screens have identified host factors regulating severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) replication. Here, we conducted a meta-analysis of these screens, which showed a high level of cell-type specificity of the identified hits, highlighting the necessity of additional models to uncover the full landscape of host factors. Thus, we performed genome-wide KO and activation screens in Calu-3 lung cells and KO screens in Caco-2 colorectal cells, followed by secondary screens in four human cell lines. This revealed host-dependency factors, including AP1G1 adaptin and ATP8B1 flippase, as well as inhibitors, including mucins. Interestingly, some of the identified genes also modulate Middle East respiratory syndrome coronavirus (MERS-CoV) and seasonal human coronavirus (HCoV) (HCoV-NL63 and HCoV-229E) replication. Moreover, most genes had an impact on viral entry, with AP1G1 likely regulating TMPRSS2 activity at the plasma membrane. These results demonstrate the value of multiple cell models and perturbational modalities for understanding SARS-CoV-2 replication and provide a list of potential targets for therapeutic interventions.
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