ArticleNucleic acids research2019
KSHV RNA-binding protein ORF57 inhibits P-body formation to promote viral multiplication by interaction with Ago2 and GW182.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- ORF57/MTA in KSHV Biology and Pathogenesis: Update From 2015.Journal of medical virology · 2026Review
- The anti-viral protein Shiftless blocks p-body formation during KSHV infection.The Journal of general virology · 2026Article
- Remodeling of Metabolic and Secretory Organelles During Oncogenic and Oncomodulatory Viral Infections.Viruses · 2026Review
- Article
- Induction of translation-suppressive G3BP1hLife · 2025Article
- Article
- Review
- KSHV promotes oncogenic FOS to inhibit nuclease AEN and transactivate RGS2 for AKT phosphorylation.bioRxiv : the preprint server for biology · 2024Article
- Human herpesvirus 8 ORF57 protein is able to reduce TDP-43 pathology: network analysis identifies interacting pathways.Human molecular genetics · 2023Article
- RNA helicase DDX6 and scaffold protein GW182 in P-bodies promote biogenesis of stress granules.Nucleic acids research · 2023Article
- Cellular state landscape and herpes simplex virus type 1 infection progression are connected.Nature communications · 2023Article
- Application of the CDK9 inhibitor FIT-039 for the treatment of KSHV-associated malignancy.BMC cancer · 2023Article
- Shiftless Restricts Viral Gene Expression and Influences RNA Granule Formation during Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Journal of virology · 2022Article
- Genome-wide regulation of KSHV RNA splicing by viral RNA-binding protein ORF57.PLoS pathogens · 2022Article
- A Panel of Kaposi's Sarcoma-Associated Herpesvirus Mutants in the Polycistronic Kaposin Locus for Precise Analysis of Individual Protein Products.Journal of virology · 2022Article
- Protein-RNA Interactome Analysis Reveals Wide Association of Kaposi's Sarcoma-Associated Herpesvirus ORF57 with Host Noncoding RNAs and Polysomes.Journal of virology · 2022Article
- Epstein-Barr Virus BGLF2 commandeers RISC to interfere with cellular miRNA function.PLoS pathogens · 2022Article
- Viral Manipulation of a Mechanoresponsive Signaling Axis Disassembles Processing Bodies.Molecular and cellular biology · 2021Article
- Enterovirus 71 2A Protease Inhibits P-Body Formation To Promote Viral RNA Synthesis.Journal of virology · 2021Article
- RNA Granules in Antiviral Innate Immunity: A Kaposi's Sarcoma-Associated Herpesvirus Journey.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Cellular non-membranous RNA-granules, P-bodies (RNA processing bodies, PB) and stress granules (SG), are important components of the innate immune response to virus invasion. Mechanisms governing how a virus modulates PB formation remain elusive. Here, we report the important roles of GW182 and DDX6, but not Dicer, Ago2 and DCP1A, in PB formation, and that Kaposi's sarcoma-associated herpesvirus (KSHV) lytic infection reduces PB formation through several specific interactions with viral RNA-binding protein ORF57. The wild-type ORF57, but not its N-terminal dysfunctional mutant, inhibits PB formation by interacting with the N-terminal GW-domain of GW182 and the N-terminal domain of Ago2, two major components of PB. KSHV ORF57 also induces nuclear Ago2 speckles. Homologous HSV-1 ICP27, but not EBV EB2, shares this conserved inhibitory function with KSHV ORF57. By using time-lapse confocal microscopy of HeLa cells co-expressing GFP-tagged GW182, we demonstrated that viral ORF57 inhibits primarily the scaffolding of GW182 at the initial stage of PB formation. Consistently, KSHV-infected iSLK/Bac16 cells with reduced GW182 expression produced far fewer PB and SG, but 100-fold higher titer of infectious KSHV virions when compared to cells with normal GW182 expression. Altogether, our data provide the first evidence that a DNA virus evades host innate immunity by encoding an RNA-binding protein that promotes its replication by blocking PB formation.
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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.