ArticleCell reports2019
EPS8 Facilitates Uncoating of Influenza A Virus.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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.
Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- A CRISPR activation screen identifies CH25H as a restriction factor against influenza viruses by targeting accessible cholesterol.Emerging microbes & infections · 2026Article
- Global remodeling of ADP-ribosylation by PARP1 suppresses influenza A virus infection.Nature communications · 2025Article
- IFIT3 RNA-binding activity promotes influenza A virus infection and translation efficiency.Journal of virology · 2025Article
- ANP32 proteins from ticks and vertebrates are key host factors for replication of Bourbon virus across species.Journal of virology · 2025Article
- Influenza A virus subverts the LC3-pericentrin dynein adaptor complex for host cytoplasm entry.Science advances · 2025Article
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- IFIT3 RNA-binding activity promotes influenza A virus infection and translation efficiency.bioRxiv : the preprint server for biology · 2025Article
- Antiviral strategies against influenza virus: an update on approved and innovative therapeutic approaches.Cellular and molecular life sciences : CMLS · 2025Review
- Incompatible packaging signals and impaired protein functions hinder reassortment of bat H17N10 or H18N11 segment 7 with human H1N1 influenza A viruses.Journal of virology · 2024Article
- Cryptic proteins translated from deletion-containing viral genomes dramatically expand the influenza virus proteome.Nucleic acids research · 2024Article
- Cryptic proteins translated from deletion-containing viral genomes dramatically expand the influenza virus proteome.bioRxiv : the preprint server for biology · 2024Article
- Pathogenicity and virulence of influenza.Virulence · 2023Review
- ABTB1 facilitates the replication of influenza A virus by counteracting TRIM4-mediated degradation of viral NP protein.Emerging microbes & infections · 2023Article
- Pathogen-driven CRISPR screens identify TREX1 as a regulator of DNA self-sensing during influenza virus infection.Cell host & microbe · 2023Article
- Article
- Pathogen-driven CRISPR screens identify TREX1 as a regulator of DNA self-sensing during influenza virus infection.bioRxiv : the preprint server for biology · 2023Article
- Influenza A Virus: Cellular Entry.Sub-cellular biochemistry · 2023Article
- Alternative splicing liberates a cryptic cytoplasmic isoform of mitochondrial MECR that antagonizes influenza virus.PLoS biology · 2022Article
- An anti-influenza combined therapy assessed by single cell RNA-sequencing.Communications biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
All viruses balance interactions between cellular machinery co-opted to support replication and host factors deployed to halt the infection. We use gene correlation analysis to perform an unbiased screen for host factors involved in influenza A virus (FLUAV) infection. Our screen identifies the cellular factor epidermal growth factor receptor pathway substrate 8 (EPS8) as the highest confidence pro-viral candidate. Knockout and overexpression of EPS8 confirm its importance in enhancing FLUAV infection and titers. Loss of EPS8 does not affect virion attachment, uptake, or fusion. Rather, our data show that EPS8 specifically functions during virion uncoating. EPS8 physically associates with incoming virion components, and subsequent nuclear import of released ribonucleoprotein complexes is significantly delayed in the absence of EPS8. Our study identifies EPS8 as a host factor important for uncoating, a crucial step of FLUAV infection during which the interface between the virus and host is still being discovered.
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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.