ArticleProceedings of the National Academy of Sciences of the United States of America2022
Viral evasion of PKR restriction by reprogramming cellular stress granules.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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Who cites it
32 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Reprogramming innate immunity through viral interference: A double-edged strategy for enhancing and containing gene therapies.Molecular therapy. Nucleic acids · 2026Review
- Equine infectious anemia virus blocks interferon responses through Rev-mediated activation of the stress granule-PKR-eIF2α pathway.PLoS pathogens · 2026Article
- The Role of Stress Granules in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2026Review
- Molecular Regulation of HIV-1 Expression and Persistence Across Diverse Cellular Reservoirs.International journal of molecular sciences · 2026Review
- Targeting biomolecular condensates: beyond dissolution.BMC biology · 2026Review
- PRRSV-2 impedes lysosomes from eliminating secondary infected bacteria.PLoS pathogens · 2026Article
- Review
- In Vitro Characterization of Vaccine Strain-like Porcine Reproductive and Respiratory Syndrome Virus Strains Isolated from Weaned Pigs Exhibiting Respiratory Symptoms.Pathogens (Basel, Switzerland) · 2025Article
- The SHFV nsp2 and nucleocapsid proteins recruit G3BP1 to sites of viral replication, but stress granules are not induced by the infection.Journal of virology · 2025Article
- THAP11-mediated K48- and K63-linked ubiquitination is essential for the degradation of porcine reproductive and respiratory syndrome virus nonstructural protein 1β.Cellular and molecular life sciences : CMLS · 2025Article
- Multi-Faceted Roles of Stress Granules in Viral Infection.Microorganisms · 2025Review
- Strategies and scheming: the war between PRRSV and host cells.Virology journal · 2025Review
- IFN alpha inducible protein 27 (IFI27) acts as a positive regulator of PACT-dependent PKR activation after RNA virus infections.PLoS pathogens · 2025Article
- Pseudorabies virus IE180 protein hijacks G3BPs into the nucleus to inhibit stress granule formation.Journal of virology · 2025Article
- Article
- The strategies and mechanisms of enteroviruses to evade innate immunity and the vaccine progress of enteroviruses.Frontiers in cellular and infection microbiology · 2025Review
- Paradigm shift: PRRSV-mediated active remodeling of the host immune system-From epigenetic domestication to functional hijacking.Frontiers in microbiology · 2025Article
- Proteome-wide characterization of PTMs reveals host cell responses to viral infection and identifies putative antiviral drug targets.Frontiers in immunology · 2025Review
- Pulling back the mitochondria's iron curtain.npj metabolic health and disease · 2025Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinase R (PKR) is a critical host restriction factor against invading viral pathogens. However, this molecule is inactivated in the cells infected with porcine reproductive and respiratory syndrome virus (PRRSV), an economically devastating pathogen to the world swine industry. Here, we report that this event is to suppress cellular inflammation and is mediated by the viral replicase protein nsp1β. We show that nsp1β is a stress-responsive protein, enters virus-induced stress granules (SGs) during infection, and repurposes SGs into a proviral platform, where it co-opts the SG core component G3BP1 to interact with PKR in a regulated manner. RNA interference silencing of G3BP1 or mutation of specific nsp1β residues (VS19GG) can abolish the antagonization of PKR activation. The viral mutant carrying the corresponding mutations induces elevated level of PKR phosphorylation and pronounced production of inflammatory cytokines (e.g., tumor necrosis factor-α, interleukin [IL]-6, and IL-8), whereas small-interfering RNA knockdown of PKR or treatment with C16, a PKR inhibitor, blocks this effect. Thus, PRRSV has evolved a unique strategy to evade PKR restriction to suppress host inflammatory responses.
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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.