ArticlePloS one2014
A loss of function analysis of host factors influencing Vaccinia virus replication by RNA interference.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 33 citations in OpenAlex.
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Vaccinia virus Tiantan strain blocks host antiviral innate immunity and programmed cell death by disrupting gene expression.Biosafety and health · 2024Article
- Vaccinia virus subverts xenophagy through phosphorylation and nuclear targeting of p62.The Journal of cell biology · 2024Article
- Unearthing the role of septins in viral infections.Bioscience reports · 2024Review
- Identification of β2 microglobulin, the product of B2M gene, as a Host Factor for Vaccinia Virus Infection by Genome-Wide CRISPR genetic screens.PLoS pathogens · 2022Article
- Vaccinia virus hijacks ESCRT-mediated multivesicular body formation for virus egress.Life science alliance · 2021Article
- Discovering antiviral restriction factors and pathways using genetic screens.The Journal of general virology · 2021Review
- Septins in Infections: Focus on Viruses.Pathogens (Basel, Switzerland) · 2021Review
- Identification of oncolytic vaccinia restriction factors in canine high-grade mammary tumor cells using single-cell transcriptomics.PLoS pathogens · 2020Article
- Conserved Oligomeric Golgi (COG) Complex Proteins Facilitate Orthopoxvirus Entry, Fusion and Spread.Viruses · 2020Article
- DNA mismatch repair is required for the host innate response and controls cellular fate after influenza virus infection.Nature microbiology · 2019Article
- Carbenoxolone-mediated cytotoxicity inhibits Vaccinia virus replication in a human keratinocyte cell line.Scientific reports · 2018Article
- Septins suppress the release of vaccinia virus from infected cells.The Journal of cell biology · 2018Article
- Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy.Journal of visualized experiments : JoVE · 2018Article
- Ubiquitin-Proteasome System Is Required for Efficient Replication of Singapore Grouper Iridovirus.Frontiers in microbiology · 2018Article
- The Host Restriction Factor Interferon-Inducible Transmembrane Protein 3 Inhibits Vaccinia Virus Infection.Frontiers in immunology · 2018Article
- Interaction of Recombinant Gallus gallus SEPT5 and Brain Proteins of H5N1-Avian Influenza Virus-Infected Chickens.Proteomes · 2017Article
- Monkeypox Virus Host Factor Screen Using Haploid Cells Identifies Essential Role of GARP Complex in Extracellular Virus Formation.Journal of virology · 2017Article
- Vaccinia Virus Uses Retromer-Independent Cellular Retrograde Transport Pathways To Facilitate the Wrapping of Intracellular Mature Virions during Virus Morphogenesis.Journal of virology · 2016Article
- AMP-activated Protein Kinase As a Target For Pathogens: Friends Or Foes?Current drug targets · 2016Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Vaccinia virus (VACV) is a large, cytoplasmic, double-stranded DNA virus that requires complex interactions with host proteins in order to replicate. To explore these interactions a functional high throughput small interfering RNA (siRNA) screen targeting 6719 druggable cellular genes was undertaken to identify host factors (HF) influencing the replication and spread of an eGFP-tagged VACV. The experimental design incorporated a low multiplicity of infection, thereby enhancing detection of cellular proteins involved in cell-to-cell spread of VACV. The screen revealed 153 pro- and 149 anti-viral HFs that strongly influenced VACV replication. These HFs were investigated further by comparisons with transcriptional profiling data sets and HFs identified in RNAi screens of other viruses. In addition, functional and pathway analysis of the entire screen was carried out to highlight cellular mechanisms involved in VACV replication. This revealed, as anticipated, that many pro-viral HFs are involved in translation of mRNA and, unexpectedly, suggested that a range of proteins involved in cellular transcriptional processes and several DNA repair pathways possess anti-viral activity. Multiple components of the AMPK complex were found to act as pro-viral HFs, while several septins, a group of highly conserved GTP binding proteins with a role in sequestering intracellular bacteria, were identified as strong anti-viral VACV HFs. This screen has identified novel and previously unexplored roles for cellular factors in poxvirus replication. This advancement in our understanding of the VACV life cycle provides a reliable knowledge base for the improvement of poxvirus-based vaccine vectors and development of anti-viral theraputics.
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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.