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

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

PROVIDER: PRJNA592532 | ENA |

REPOSITORIES: ENA

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

Project description: Not available

| S-EPMC6952391 | biostudies-literature

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-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

A Virus-Packageable CRISPR System Identifies Host Dependency Factors Co-opted by Multiple HIV-1 Strains

Project description:The goal of this CRISPR-based screen (HIV-CRISPR) is to identify HIV-1 dependency factors by evaluating multiple pathways simultaneously. Here are Illumina sequencing data and counts files from HIV-CRISPR screens using a guide RNA library targeting the whole genome (TKOv3), a custom guide RNA library targeting human epigenome genes (HuEpi), a custom guide RNA library targeting interferon-stimulated genes (PIKA), and a custom guide RNA library of genes containing of a subset of each of the aforementioned libraries designed to target human dependency factors (HIVDEP). The HIV-CRISPR screens described here were performed in clonal ZAP knockout Jurkat cell lines as ZAP inhibition of the HIV-CRISPR vector has been previously described (PMID: 30520725).

2023-01-26 | GSE223326 | GEO

A genome-wide CRISPR screen identifies a restricted set of HIV host dependency factors.

Project description: Not available

| S-EPMC5511375 | biostudies-literature

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

| PRJNA436088 | ENA

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

Project description: Not available

| S-EPMC5939577 | biostudies-literature

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

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 screen of HIV dependency factors reveals CCNT1 is non-essential in T cells but required for HIV-1 reactivation from latency [CRISPR]

Project description:We sought to explore the hypothesis that host factors required for HIV-1 replication also play a role in latency reversal. Using a CRISPR gene library of putative HIV dependency factors, we performed a screen to identify genes required for latency reactivation. We identified several HIV- 1 dependency factors that play a key role in HIV-1 latency reactivation including ELL, UBE2M, TBL1XR1, HDAC3, AMBRA1, and ALYREF. Knockout of Cyclin T1 (CCNT1), a component of the P-TEFb complex important for transcription elongation, was the top hit in the screen and had the largest effect on HIV latency reversal with a wide variety of latency reversal agents. Moreover, CCNT1 knockout prevents latency reactivation in a primary CD4+ T cell model of HIV latency without affecting activation of these cells. RNA sequencing data showed that CCNT1 regulates HIV-1 proviral genes to a larger extent than any other host gene and had no significant effects on RNA transcripts in primary T cells after activation. We conclude that CCNT1 function is redundant in T cells but is absolutely required for HIV latency reversal.

2023-08-15 | GSE240894 | GEO

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