ArticleCell host & microbe2012
Dynamic oscillation of translation and stress granule formation mark the cellular response to virus infection.
Article in Cell host & microbe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
123 citing papers in PubMed, 185 citations in OpenAlex.
- Stress granules at the crossroads of the proteostasis network.RNA biology · 2026Review
- Assembly of lipid droplet-associated ring structures in hepatitis C virus-infected cells via liquid-liquid phase separation (LLPS) and non-LLPS mechanisms.Journal of virology · 2026Article
- Stress granule phase separation in stress-responsive cytosolic extract-in-oil droplets.Nature communications · 2026Article
- Evolution of a truncated nucleocapsid protein enhances SARS-CoV-2 fitness by suppressing antiviral responses.PLoS biology · 2026Article
- Cellular Biology: Virus-Host Interactions and RNA Structure and Function.Current topics in microbiology and immunology · 2026Review
- Ultrack: pushing the limits of cell tracking across biological scales.Nature methods · 2025Article
- Granular Insights on Innate and Intrinsic Immunity to Flaviviruses.Microorganisms · 2025Review
- Emerging roles of stress granules in liver diseases: a comprehensive review.Frontiers in cell and developmental biology · 2025Review
- Stress Granules in Infectious Disease: Cellular Principles and Dynamic Roles in Immunity and Organelles.International journal of molecular sciences · 2024Review
- A closer look at mammalian antiviral condensates.Biochemical Society transactions · 2024Review
- Article
- Substrate recruitment via eIF2γ enhances catalytic efficiency of a holophosphatase that terminates the integrated stress response.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Interaction between host G3BP and viral nucleocapsid protein regulates SARS-CoV-2 replication and pathogenicity.Cell reports · 2024Article
- Avian Influenza A Viruses Modulate the Cellular Cytoskeleton during Infection of Mammalian Hosts.Pathogens (Basel, Switzerland) · 2024Review
- Emerging roles of the Protein Phosphatase 1 (PP1) in the context of viral infections.Cell communication and signaling : CCS · 2024Review
- Copy-back viral genomes induce a cellular stress response that interferes with viral protein expression without affecting antiviral immunity.PLoS biology · 2023Article
- Stress Granules as Causes and Consequences of Translation Suppression.Antioxidants & redox signaling · 2023Review
- MIA is an open-source standalone deep learning application for microscopic image analysis.Cell reports methods · 2023Article
- Biomolecular phase separation in stress granule assembly and virus infection.Acta biochimica et biophysica Sinica · 2023Article
- Endosomal egress and intercellular transmission of hepatic ApoE-containing lipoproteins and its exploitation by the hepatitis C virus.PLoS pathogens · 2023Article
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Virus infection-induced global protein synthesis suppression is linked to assembly of stress granules (SGs), cytosolic aggregates of stalled translation preinitiation complexes. To study long-term stress responses, we developed an imaging approach for extended observation and analysis of SG dynamics during persistent hepatitis C virus (HCV) infection. In combination with type 1 interferon, HCV infection induces highly dynamic assembly/disassembly of cytoplasmic SGs, concomitant with phases of active and stalled translation, delayed cell division, and prolonged cell survival. Double-stranded RNA (dsRNA), independent of viral replication, is sufficient to trigger these oscillations. Translation initiation factor eIF2α phosphorylation by protein kinase R mediates SG formation and translation arrest. This is antagonized by the upregulation of GADD34, the regulatory subunit of protein phosphatase 1 dephosphorylating eIF2α. Stress response oscillation is a general mechanism to prevent long-lasting translation repression and a conserved host cell reaction to multiple RNA viruses, which HCV may exploit to establish persistence.
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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.