Evidence map›Paper›PMID 28813663›Full record

ArticleCell reports2017

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

Brook E Heaton, Edward M Kennedy, Rebekah E Dumm, Alfred T Harding, Matthew T Sacco, David Sachs, Nicholas S Heaton

Abstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

94 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. FUT1- and GAL3ST2-mediated cellular glycan remodeling broadly restricts sialic acid-dependent viral infections.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  20. Computational Analysis of Virus-Host Interactomes.Methods in molecular biology (Clifton, N.J.) · 2025
    Review

34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Brook E HeatonDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Edward M KennedyDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Rebekah E DummDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Alfred T HardingDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Matthew T SaccoDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
David SachsDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Nicholas S HeatonDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: nicholas.heaton@duke.edu.

Funding

ORGANIZATION AND FUNCTIONS OF CELLULAR STRUCTUREST32GM007184 · NIGMS · DUKE UNIVERSITY · PI JINKS-ROBERTSON, SUE · 1985 to 2019
$18.2M
Viral Oncology Training GrantT32CA009111 · NCI · DUKE UNIVERSITY · PI LUFTIG, MICAH A. · 1985 to 2023
$8.9M
Survival of influenza A virus infected cells and effects on pathogenesisK22AI116509 · NIAID · DUKE UNIVERSITY · PI HEATON, NICHOLAS S · 2016 to 2017
$267k
NCI NIH HHS T32 CA009111NIAID NIH HHS K22 AI116509NIGMS NIH HHS T32 GM007184
6 · The paper itself

Abstract

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.

Indexed as

CRISPR-Cas SystemsA549 CellsAnimalsCarbohydrate SequenceDogsGene ExpressionGenes, ReporterGenetic EngineeringGenome, HumanHEK293 CellsHigh-Throughput Screening AssaysHost-Parasite InteractionsHumansInfluenza A virusLuciferasesMadin Darby Canine Kidney Cellsbeta-1,4-N-acetyl-galactosaminyl transferase 2LuciferasesN-AcetylgalactosaminyltransferasesPolysaccharidesReceptors, VirusSialic Acidsavian influenza virusB4GALNT2CRISPR activation screenglycotransferaseinfluenza A virus

Identifiers

PMID28813663
PMCPMC5568676

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Registered trials

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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.