ArticleVirology journal2013
Differential unfolded protein response during Chikungunya and Sindbis virus infection: CHIKV nsP4 suppresses eIF2α phosphorylation.
Article in Virology journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 103 citations in OpenAlex.
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- Protein kinase R-like ER kinase (PERK) is involved in the endoplasmic reticulum stress response of its psyllid vector toMicrobiology spectrum · 2026Article
- Rewiring of host cell signaling in chikungunya virus infection: a mechanism for pathogenesis and therapeutic approaches.Archives of microbiology · 2026Review
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- Chikungunya Replication and Infection Is Dependent upon and Alters Cellular Hexosylceramide Levels in Vero Cells.Viruses · 2025Article
- Alphavirus nsP2: A Multifunctional Regulator of Viral Replication and Promising Target for Anti-Alphavirus Therapies.Reviews in medical virology · 2025Review
- The sticky business of Alphavirus capsid-host interactions.Trends in microbiology · 2025Review
- Identification of RACK1 as a novel regulator of non-structural protein 4 of chikungunya virus.Acta biochimica et biophysica Sinica · 2024Article
- Translational Control of Alphavirus-Host Interactions: Implications in Viral Evolution, Tropism and Antiviral Response.Viruses · 2024Review
- Unraveling the complex interplay: immunopathology and immune evasion strategies of alphaviruses with emphasis on neurological implications.Frontiers in cellular and infection microbiology · 2024Review
- Toxoplasma-host endoplasmic reticulum interaction: HowCurrent research in microbial sciences · 2024Review
- Pharmacological Manipulation of UPR: Potential Antiviral Strategy Against Chikungunya Virus.Indian journal of microbiology · 2022Article
- Investigation of the Crosstalk between GRP78/PERK/ATF-4 Signaling Pathway and Renal Apoptosis Induced by Nephropathogenic Infectious Bronchitis Virus Infection.Journal of virology · 2022Article
- Understanding Molecular Pathogenesis with Chikungunya Virus Research Tools.Current topics in microbiology and immunology · 2022Review
- Innate immune evasion by alphaviruses.Frontiers in immunology · 2022Review
- Small Molecule Inhibitors Targeting Chikungunya Virus.Current topics in microbiology and immunology · 2022Review
- Paradoxical effects of DNA tumor virus oncogenes on epithelium-derived tumor cell fate during tumor progression and chemotherapy response.Signal transduction and targeted therapy · 2021Article
- Alphavirus Virulence Determinants.Pathogens (Basel, Switzerland) · 2021Review
14 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chikungunya (CHIKV) and Sindbis (SINV) are arboviruses belonging to the alphavirus genus within the Togaviridae family. They cause frequent epidemics of febrile illness and long-term arthralgic sequelae that affect millions of people each year. Both viruses replicate prodigiously in infected patients and in vitro in mammalian cells, suggesting some level of control over the host cellular translational machinery that senses and appropriately directs the cell's fate through the unfolded protein response (UPR). The mammalian UPR involves BIP (or GRP78), the master sensor in the endoplasmic reticulum (ER) together with the three downstream effector branches: inositol-requiring ser/thr protein kinase/endonuclease (IRE-1), PKR-like ER resident kinase (PERK) and activating transcription factor 6 (ATF-6). Through careful analysis of CHIKV and SINV infections in cell culture we found that the former selectively activates ATF-6 and IRE-1 branches of UPR and suppresses the PERK pathway. By separately expressing each of the CHIKV proteins as GFP-fusion proteins, we found that non-structural protein 4 (nsP4), which is a RNA-dependent-RNA polymerase, suppresses the serine-51 phosphorylation of eukaryotic translation initiation factor, alpha subunit (eIF2α), which in turn regulates the PERK pathway. This study provides insight into a mechanism by which CHIKV replication responds to overcome the host UPR machinery.
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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 OpenQuestion graph.