ArticleJournal of virology2010
The African swine fever virus DP71L protein recruits the protein phosphatase 1 catalytic subunit to dephosphorylate eIF2alpha and inhibits CHOP induction but is dispensable for these activities during virus infection.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 119 citations in OpenAlex.
- African Swine Fever Virus DP71L Protein Inhibits Dextran Sulfate Sodium (DSS)-Induced Murine Colitis.Viruses · 2026Article
- The ASFV CD2v protein inhibits apoptosis by inducing proteasomal degradation of BimJournal of virology · 2026Article
- The Prospects and Challenges of Live Attenuated Vaccines Against African Swine Fever Virus in Vietnam.Vaccines · 2026Review
- The CP312R protein of African swine fever virus inhibits host protein translation via the BiP/PERK/eIF2α pathway.Veterinary research · 2026Article
- ASFV MGF110-7L Inhibits eIF4G1 Expression via Endoplasmic Reticulum Stress to Block Host Translation.Viruses · 2026Article
- Immunoevasion strategies for African swine fever virus: Modulation of antigen presentation pathways.Virulence · 2025Review
- Dynamic Gene Network Alterations and Identification of Key Genes in the Spleen During African Swine Fever Virus (ASFV) Infection.Life (Basel, Switzerland) · 2025Article
- African swine fever virus pB318L suppresses inflammatory response by inhibiting NF-κB activation and NLRP3 inflammasome formation.PLoS pathogens · 2025Article
- African swine fever virus A179L inhibits interferon induced transmembrane protein 1 activation of NF-κB pathway.Cell communication and signaling : CCS · 2025Article
- Multi-Faceted Roles of Stress Granules in Viral Infection.Microorganisms · 2025Review
- Advances in African swine fever virus molecular biology and host interactions contributing to new tools for control.Journal of virology · 2025Review
- Inhibition of STING-mediated type I IFN signaling by African swine fever virus DP71L.Veterinary research · 2025Article
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- African swine fever virus enhances viral replication by increasing intracellular reduced glutathione levels, which suppresses stress granule formation.Veterinary research · 2024Article
- Protein phosphatase 1 suppresses PKR/EIF2α signaling during human cytomegalovirus infection.Journal of virology · 2024Article
- The NS2B-PP1α-eIF2α axis: Inhibiting stress granule formation and Boosting Zika virus replication.PLoS pathogens · 2024Article
- Identification of host proteins that interact with African swine fever virus pE301R.Engineering microbiology · 2024Article
- African swine fever virus proteins against host antiviral innate immunity and their implications for vaccine development.Open veterinary journal · 2024Review
- The transcriptomic insight into the differential susceptibility of African Swine Fever in inbred pigs.Scientific reports · 2024Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The African swine fever virus (ASFV) DP71L protein is present in all isolates as either a short form of 70 to 72 amino acids or a long form of about 184 amino acids, and both of these share sequence similarity to the C-terminal domain of the herpes simplex virus ICP34.5 protein and cellular protein GADD34. In the present study we expressed DP71L in different mammalian cells and demonstrated that DP71L causes dephosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2α) in resting cells and during chemical-induced endoplasmic reticulum stress and acts to enhance expression of cotransfected reporter genes. We showed that DP71L binds to all the three isoforms (α, β, and γ) of the protein phosphatase 1 catalytic subunit (PP1c) and acts by recruiting PP1c to eIF2α. We also showed that DP71L inhibits the induction of ATF4 and its downstream target, CHOP. We investigated the eIF2α phosphorylation status and induction of CHOP in porcine macrophages infected by two ASFV field isolates, Malawi Lil20/1 and Benin 97/1, and two DP71L deletion mutants, MalawiΔNL and E70ΔNL. Our results showed that deletion of the DP71L gene did not cause an increase in the level of eIF2α phosphorylation or induction of CHOP, indicating that DP71L is not the only factor required by the virus to control the phosphorylation level of eIF2α during infection. We therefore hypothesize that ASFV has other mechanisms to prevent the eIF2α phosphorylation and the subsequent protein synthesis inhibition.
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