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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

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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.

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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 (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.

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CRISPR editing of candidate host factors that impact influenza A virus infection

Project description:Influenza A virus (IAV) is a respiratory pathogen with a segmented negative-sense RNA genome that is capable of causing epidemics and pandemics. The error-prone nature of the IAV polymerase results in antigenic drift and antigenic shift which contribute to low vaccine efficacy and escape from antivirals. The host factors required for the complete IAV infectious cycle have not been fully identified. Here, we examined select host factors that were identified by independent CRISPR screens as candidate contributors to IAV infectivity. We performed CRISPR-mediated knockout of cytidine monophosphate N-acetylneuraminic acid synthetase (CMAS) as well as CRISPR-mediated overexpression of beta-1,4 N-acetylgalactosaminyltransferase 2 (B4GALNT2) and adenosine deaminase acting on RNA 1 (ADAR1) in the human bronchial epithelial A549 cell line and evaluated for reduction of IAV infection. We confirmed that the knockout of CMAS or overexpression of B4GALNT2 restricts IAV infection by diminishing binding to the cell surface. While ADAR1 overexpression did not significantly inhibit IAV replication, it had a pro-viral effect with coxsackie B virus infection. Taken together, these data provide insight into how host factors identified in CRISR screens can modulate IAV infection and be utilized to further understand the IAV life cycle and for developing antiviral strategies.

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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: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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