ArticleJournal of virology2021
A novel function of African Swine Fever Virus pE66L in inhibition of host translation by the PKR/eIF2α pathway.
Article in Journal of virology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Loss of ribosomal protein RPL22 restricts African swine fever virus replication by inducing PERK-dependent ER stress.Emerging microbes & infections · 2026Article
- The CP312R protein of African swine fever virus inhibits host protein translation via the BiP/PERK/eIF2α pathway.Veterinary research · 2026Article
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- Nuclear factor erythroid 2-related factor: potential use as a therapeutic strategy for viral infections.Archives of microbiology · 2026Review
- Role of g5Rp in African swine fever virus replication: disruption of host translation and autophagy.Journal of virology · 2026Article
- The antagonistic coevolution between Pseudomonas sivasensis W-6 and the cold-adapted phage VW6S.Antonie van Leeuwenhoek · 2026Article
- Structural and Functional Analysis of ASFV pI73R Reveals GNB1 Binding and Host Gene Modulation.International journal of molecular sciences · 2025Article
- Immunoevasion strategies for African swine fever virus: Modulation of antigen presentation pathways.Virulence · 2025Review
- Translation of nervous necrosis virus involves eIF4E but not RPS6 phosphorylation and viral particle assembly in remodeled microtubule-organizing center.Virology journal · 2025Article
- Canine parvovirus NS1 induces host translation shutoff by reducing mTOR phosphorylation.Journal of virology · 2025Article
- Identification of host proteins that interact with African swine fever virus pE301R.Engineering microbiology · 2024Article
- Novel mutation N588 residue in the NS1 protein of feline parvovirus greatly augments viral replication.Journal of virology · 2024Article
- African swine fever virus RNA polymerase subunits C315R and H359L inhibition host translation by activating the PKR-eIF2a pathway and suppression inflammatory responses.Frontiers in microbiology · 2024Article
- African swine fever virus structural protein p17 inhibits IRF3 activation by recruiting host protein PR65A and inducing apoptotic degradation of STING.Frontiers in microbiology · 2024Article
- Functional Landscape of African Swine Fever Virus-Host and Virus-Virus Protein Interactions.Viruses · 2023Review
- Article
- African swine fever virus I73R is a critical virulence-related gene: A potential target for attenuation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- African Swine Fever Virus MGF505-7R Interacts with Interferon Regulatory Factor 9 to Evade the Type I Interferon Signaling Pathway and Promote Viral Replication.Journal of virology · 2023Article
- Evaluation of the Function of ASFV Gene E66L in the Process of Virus Replication and Virulence in Swine.Viruses · 2023Article
- Comparative genomic and transcriptomic analyses of African swine fever virus strains.Computational and structural biotechnology journal · 2023Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African swine fever virus (ASFV) is one of the most contagious and lethal viruses infecting pigs. This virus is endemic in many countries and has very recently spread to China, but no licensed vaccines or treatments are currently available. Despite extensive research, the basic question of how ASFV-encoded proteins inhibit host translation remains. Here, we examined how ASFV interfered with host translation and optimized viral gene expression. We found that 14 ASFV proteins inhibited Renilla luciferase (Rluc) activity greater than 5-fold, and the protein with the strongest inhibitory effect was pE66L, which was not previously reported. Combined with bioinformatical analysis and biochemical experiment, we determined that the transmembrane (TM) domain (amino acids 13-34) of pE66L was required for the inhibition of host gene expression. Notably, we constructed a recombinant plasmid with the TM domain linked to enhanced green fluorescent protein (EGFP) and further demonstrated that this domain broadly inhibited protein synthesis. Confocal and biochemical analyses indicated that the TM domain might help proteins locate to the endoplasmic reticulum (ER) to suppress translation though the PKR/eIF2α pathway. Deletion of the E66L gene had little effect on virus replication in macrophages, but significantly recovered host gene expression. Taken together, our findings complement studies on the host translation of ASFV proteins and suggest that ASFV pE66L induces host translation shutoff, which is dependent on activation of the PKR/eIF2α pathway.
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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.