ArticlePLoS pathogens2022
Inducible CRISPR activation screen for interferon-stimulated genes identifies OAS1 as a SARS-CoV-2 restriction factor.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 58 citations in OpenAlex.
- A knockout screening platform for interferon-stimulated genes in respiratory cells identifies LY6E as a dominant antiviral effector against coronaviruses.bioRxiv : the preprint server for biology · 2026Article
- METTL3 promotes human coronavirus replication through an interferon-independent mechanism.bioRxiv : the preprint server for biology · 2026Article
- Alternative splicing broadens antiviral diversity at the human OAS2 locus.The EMBO journal · 2026Article
- Dietary Glycerol Monolaurate Enhances Growth and Immune Function in Calves via Hepatic Immunometabolic Reprogramming.Veterinary sciences · 2026Article
- The ISG Atlas: a loss-of-function analysis characterizes antiviral properties of interferon stimulated genes.Nature communications · 2026Article
- From CRISPR functional genomics to synthetic interventions: engineering antiviral strategies.Journal of virology · 2026Review
- SARS-CoV-2 Nsp15 facilitates immune evasion and viral replication by limiting multiple host innate immune pathways, including cGAS-STING.The Journal of general virology · 2026Article
- The OAS-RNase L pathway: Insights from experiments of nature.Science immunology · 2026Review
- Article
- Poly(A) tail dynamics, non-adenine incorporation and alternative polyadenylation shape the host transcriptome in COVID-19 pathogenesis.Scientific reports · 2025Article
- Human guanylate-binding protein (GBP) 1 inhibits replication of severe acute respiratory syndrome coronavirus 2.Journal of virology · 2025Article
- Article
- Direct pharmacological AMPK activation inhibits mucosal SARS-CoV-2 infection by reducing lipid metabolism, restoring autophagy flux and the type I IFN response.Journal of virology · 2025Article
- Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025Review
- MDA5 Is a Major Determinant of Developing Symptoms in Critically Ill COVID-19 Patients.Clinical reviews in allergy & immunology · 2024Review
- Ultrasound Control of Genomic Regulatory Toolboxes for Cancer Immunotherapy.Nature communications · 2024Article
- Review
- A basally active cGAS-STING pathway limits SARS-CoV-2 replication in a subset of ACE2 positive airway cell models.Nature communications · 2024Article
- Review
- A basally active cGAS-STING pathway limits SARS-CoV-2 replication in a subset of ACE2 positive airway cell models.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Interferons establish an antiviral state through the induction of hundreds of interferon-stimulated genes (ISGs). The mechanisms and viral specificities for most ISGs remain incompletely understood. To enable high-throughput interrogation of ISG antiviral functions in pooled genetic screens while mitigating potentially confounding effects of endogenous interferon and antiproliferative/proapoptotic ISG activities, we adapted a CRISPR-activation (CRISPRa) system for inducible ISG expression in isogenic cell lines with and without the capacity to respond to interferons. We used this platform to screen for ISGs that restrict SARS-CoV-2. Results included ISGs previously described to restrict SARS-CoV-2 and novel candidate antiviral factors. We validated a subset of these by complementary CRISPRa and cDNA expression experiments. OAS1, a top-ranked hit across multiple screens, exhibited strong antiviral effects against SARS-CoV-2, which required OAS1 catalytic activity. These studies demonstrate a high-throughput approach to assess antiviral functions within the ISG repertoire, exemplified by identification of multiple SARS-CoV-2 restriction factors.
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Registered trials
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.