ArticleVirology2019
Host Src controls gallid alpha herpesvirus 1 intercellular spread in a cellular fatty acid metabolism-dependent manner.
Article in Virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- MEK/ERK-Mediated Transcriptional Repression of Metabolic Genes Confers Host Defense AgainstMicroorganisms · 2026Article
- A functional interleukin-4 homolog is encoded in the genome of infectious laryngotracheitis virus: Unveiling a novel virulence factor.PLoS pathogens · 2025Article
- Review of respiratory syndromes in poultry: pathogens, prevention, and control measures.Veterinary research · 2025Review
- Co-Regulation Mechanism of Host p53 and Fos in Transcriptional Activation of ILTV Immediate-Early GeneMicroorganisms · 2024Article
- Characterization of the Effects of Host p53 and Fos on Gallid Alpha Herpesvirus 1 Replication.Genes · 2023Article
- Exploration of the Mechanism of the Control of Coccidiosis in Chickens Based on Network Pharmacology and Molecular Docking With the Addition of Modified Gegen Qinlian Decoction.Frontiers in veterinary science · 2022Article
- Article
- Global exploration of the metabolic requirements of gallid alphaherpesvirus 1.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral spread is considered a promising target for antiviral therapeutics, but the associated mechanisms remain unclear for gallid alpha herpesvirus 1 (ILTV). We previously identified proto-oncogene tyrosine-protein kinase Src (Src) as a crucial host determinant of ILTV infection. The present study revealed accelerated spread of ILTV upon Src inhibition. This phenomenon was independent of either viral replication or the proliferation of infected cells and could not be compromised by neutralizing antibody. Neither extracellular vesicles nor the direct cytosol-to-cytosol connections between adjacent cells contributed to the enhanced spread of ILTV upon Src inhibition. Further genome-wide transcriptional profile analyses in combination with functional validation identified fatty acid metabolism as an essential molecular event during modulation of the intercellular spread and subsequent cytopathic effect of ILTV by Src. Overall, these data suggest that Src controls the cell-to-cell spread of ILTV in a cellular fatty acid metabolism-dependent manner, which determines the virus's cytopathic effect.
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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 Socratic graph.