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A genome-wide CRISPR activation screen identifies B4GALNT2 as an inhibitory host factor for influenza virus infection

ABSTRACT: A genome-wide CRISPR activation screen identifies B4GALNT2 as an inhibitory host factor for influenza virus infection

PROVIDER: PRJNA351924 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4767050.fastq.gz	Fastqsanger.gz
	SRR4767051.fastq.gz	Fastqsanger.gz
	SRR4767052.fastq.gz	Fastqsanger.gz
	SRR4767053.fastq.gz	Fastqsanger.gz
	SRR4767054.fastq.gz	Fastqsanger.gz

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A genome-wide CRISPR activation screen identifies B4GALNT2 as an inhibitory host factor for influenza virus infection

Project description:Identification of factors to inhibit influenza virus infection

2017-07-17 | GSE89371 | GEO

A CRISPR Activation Screen Identifies a Pan-avian Influenza Virus Inhibitory Host Factor.

Project description:Influenza A virus (IAV) is a pathogen that poses significant risks to human health. It is therefore critical to develop strategies to prevent influenza disease. Many loss-of-function screens have been performed to identify the host proteins required for viral infection. However, there has been no systematic screen to identify the host factors that, when overexpressed, are sufficient to prevent infection. In this study, we used CRISPR/dCas9 activation technology to perform a genome-wide overexpression screen to identify IAV restriction factors. The major hit from our screen, B4GALNT2, showed inhibitory activity against influenza viruses with an α2,3-linked sialic acid receptor preference. B4GALNT2 overexpression prevented the infection of every avian influenza virus strain tested, including the H5, H9, and H7 subtypes, which have previously caused disease in humans. Thus, we have used CRISPR/dCas9 activation technology to identify a factor that can abolish infection by avian influenza viruses.

| S-EPMC5568676 | biostudies-literature

Genome-Wide CRISPR/Cas9 Screen Identifies Host Factors Essential for Influenza Virus Replication

Project description:The emergence of influenza A viruses (IAV) from zoonotic reservoirs poses a great threat to human health. As seasonal vaccines are ineffective against zoonotic strains, and newly transmitted viruses can quickly acquire drug resistance, there remains a need for host- directed therapeutics against IAV. Here, we performed a genome-scale CRISPR/Cas9 knockout screen in human lung epithelial cells with a human isolate of an avian H5N1 strain. Several genes involved in sialic acid biosynthesis and related glycosylation pathways were highly enriched post-H5N1 selection, including SLC35A1, a sialic acid transporter essential for IAV receptor expression and thus viral entry. Importantly, we have identified capicua (CIC) as a negative regulator of cell intrinsic immunity, as loss of CIC resulted in heightened antiviral responses and restricted replication of multiple viruses. Therefore, our study demonstrates that the CRISPR/Cas9 system can be utilized for the discovery of host factors critical for the replication of intracellular pathogens.

2018-02-28 | GSE111166 | GEO

Genome-Wide CRISPR/Cas9 Screen Identifies Host Factors Essential for Influenza Virus Replication

Project description:Genome-Wide CRISPR/Cas9 Screen Identifies Host Factors Essential for Influenza Virus Replication

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Genome-wide CRISPR screen Identifies Host Dependency Factors for Influenza A Virus Infection

Project description:Genome-wide CRISPR screen Identifies Host Dependency Factors for Influenza A Virus Infection

| PRJNA592532 | ENA

Genome-wide CRISPR screen identifies host dependency factors for influenza A virus infection.

Project description:Host dependency factors that are required for influenza A virus infection may serve as therapeutic targets as the virus is less likely to bypass them under drug-mediated selection pressure. Previous attempts to identify host factors have produced largely divergent results, with few overlapping hits across different studies. Here, we perform a genome-wide CRISPR/Cas9 screen and devise a new approach, meta-analysis by information content (MAIC) to systematically combine our results with prior evidence for influenza host factors. MAIC out-performs other meta-analysis methods when using our CRISPR screen as validation data. We validate the host factors, WDR7, CCDC115 and TMEM199, demonstrating that these genes are essential for viral entry and regulation of V-type ATPase assembly. We also find that CMTR1, a human mRNA cap methyltransferase, is required for efficient viral cap snatching and regulation of a cell autonomous immune response, and provides synergistic protection with the influenza endonuclease inhibitor Xofluza.

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Genome-wide CRISPR/Cas9 Screen Identifies Host Factors Essential for Influenza Virus Replication.

Project description:The emergence of influenza A viruses (IAVs) from zoonotic reservoirs poses a great threat to human health. As seasonal vaccines are ineffective against zoonotic strains, and newly transmitted viruses can quickly acquire drug resistance, there remains a need for host-directed therapeutics against IAVs. Here, we performed a genome-scale CRISPR/Cas9 knockout screen in human lung epithelial cells with a human isolate of an avian H5N1 strain. Several genes involved in sialic acid biosynthesis and related glycosylation pathways were highly enriched post-H5N1 selection, including SLC35A1, a sialic acid transporter essential for IAV receptor expression and thus viral entry. Importantly, we have identified capicua (CIC) as a negative regulator of cell-intrinsic immunity, as loss of CIC resulted in heightened antiviral responses and restricted replication of multiple viruses. Therefore, our study demonstrates that the CRISPR/Cas9 system can be utilized for the discovery of host factors critical for the replication of intracellular pathogens.

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Genome-wide CRISPR screen Identifies Host Dependency Factors for Influenza A Virus Infection

Project description:In this study, we performed a genome-wide CRISPR screen in A549 cells to identify host genes that are required forInfluenza A virus (IAV) infection.Amongst the identified genes, WDR7, CCDC115, TMEM199 and CMTR1 conferred strong protection against IAV infection when they were CRISPR-deleted without impacting host cell fitness. To investigate the roles of these genes on the transciptomic states of the cell, we performed bulk RNA-sequencing of WDR7, CCDC115, TMEM199 and CMTR1 polyclonal knockout cells. We found that cells lacking WDR7, CCDC115 or TMEM199 up-regulates expression of lysosomal genes due to increased nuclear translocation of Transcription factor EB (TFEB), which hampers IAV entry. In addition,we report that CRISPR deletion of CMTR1 results in increased expression of Interferon-stimulated genes (ISGs) that also plays a role inblocking IAV infection.

2019-11-30 | GSE141171 | GEO

Genome-scale CRISPR screen reveals inhibitory factors as regulatory module of HIV

Project description:Genome-scale CRISPR screen reveals inhibitory factors as regulatory module of HIV

| PRJNA768794 | ENA

A Virus-Packageable CRISPR Screen Identifies Host Factors Mediating Interferon Inhibition of HIV

Project description:Interferon (IFN) inhibits HIV replication by inducing an array of antiviral effectors. Here we describe a novel CRISPR knockout screening approach to identify the ensemble of these HIV restriction factors. We assembled a CRISPR sgRNA library specific for Interferon Stimulated Genes (ISGs) into a modified lentiviral vector that allows for packaging of sgRNA-encoding genomes in trans into budding HIV-1 particles. We observed that knockout of Zinc Antiviral Protein (ZAP) improved the performance of the screen due to ZAP-mediated inhibition of the vector. We identify a small panel of IFN-induced HIV restriction factors, including MxB, IFITM1, Tetherin/BST2 and TRIM5 which together explain the inhibitory effects of IFN on the HIV-1 LAI strain in THP-1 cells. Further, we identify novel HIV dependency factors, including SEC62 and TLR2. The ability of IFN-induced restriction factors to inhibit an HIV strain to replicate in human cells suggests that these human restriction factors are incompletely antagonized.

2018-08-17 | GSE118631 | GEO

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