ArticleVirology journal2018
The eukaryotic translation elongation factor 1A regulation of actin stress fibers is important for infectious RSV production.
Article in Virology journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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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.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Discovery and mutasynthetic optimization of ansatrienin B: A new broad-spectrum inhibitor against RNA viruses.Acta pharmaceutica Sinica. B · 2026Article
- Can plitidepsin be used as an antiviral against RSV?mSphere · 2025Article
- Multidimensional Regulatory Mechanisms and Targeting Strategies of the eEF1 Family in RNA Virus Infection.Viruses · 2025Review
- Genome-wide analysis of the soybeanFrontiers in plant science · 2024Article
- Clinically Evaluated COVID-19 Drugs with Therapeutic Potential for Biological Warfare Agents.Microorganisms · 2023Review
- The eEF1 family of mammalian translation elongation factors.BBA advances · 2023Article
- Actin dynamics in protein homeostasis.Bioscience reports · 2022Review
- Article
- An overview on tumor treating fields (TTFields) technology as a new potential subsidiary biophysical treatment for COVID-19.Drug delivery and translational research · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Cellular protein eukaryotic translation elongation factor 1A (eEF1A) is an actin binding protein that plays a role in the formation of filamentous actin (F-actin) bundles. F-Actin regulates multiple stages of respiratory syncytial virus (RSV) replication including assembly and budding. Our previous study demonstrated that eEF1A knock-down significantly reduced RSV replication. Here we investigated if the eEF1A function in actin bundle formation was important for RSV replication and release. To investigate this, eEF1A function was impaired in HEp-2 cells by either knock-down of eEF1A with siRNA, or treatment with an eEF1A inhibitor, didemnin B (Did B). Cell staining and confocal microscopy analysis showed that both eEF1A knock-down and treatment with Did B resulted in disruption of cellular stress fiber formation and elevated accumulation of F-actin near the plasma membrane. When treated cells were then infected with RSV, there was also reduced formation of virus-induced cellular filopodia. Did B treatment, similarly to eEF1A knock-down, reduced the release of infectious RSV, but unlike eEF1A knock-down, did not significantly affect RSV genome replication. The lower infectious virus production in Did B treated cells also reduced RSV-induced cell death. In conclusion, the cellular factor eEF1A plays an important role in the regulation of F-actin stress fiber formation required for RSV assembly and release.
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Identifiers
What OpenQuestion holds
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.