ArticleJournal of virology2012
Hepatitis C virus (HCV) induces formation of stress granules whose proteins regulate HCV RNA replication and virus assembly and egress.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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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
84 citing papers in PubMed, 117 citations in OpenAlex.
- 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
- 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
- miRNAs Involvement in Modulating Signalling Pathways Involved in Ros-Mediated Oxidative Stress in Melanoma.Antioxidants (Basel, Switzerland) · 2024Review
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- Unraveling the dynamics of hepatitis C virus adaptive mutations and their impact on antiviral responses in primary human hepatocytes.Journal of virology · 2024Article
- RNA binding protein TIAR modulates HBV replication by tipping the balance of pgRNA translation.Signal transduction and targeted therapy · 2023Article
- Ribonucleoprotein Granules: Between Stress and Transposable Elements.Biomolecules · 2023Review
- Development of FRET and Stress Granule Dual-Based System to Screen for Viral 3C Protease Inhibitors.Molecules (Basel, Switzerland) · 2023Article
- Article
- Review
- Stress granules: potential therapeutic targets for infectious and inflammatory diseases.Frontiers in immunology · 2023Review
- Cell-Type-Dependent Role for nsP3 Macrodomain ADP-Ribose Binding and Hydrolase Activity during Chikungunya Virus Infection.Viruses · 2022Article
- T-Cell Intracellular Antigen 1-Like Protein in Physiology and Pathology.International journal of molecular sciences · 2022Review
- Investigating the Human Host-ssRNA Virus Interaction Landscape Using the SMEAGOL Toolbox.Viruses · 2022Article
- Role of Stress Granules in Suppressing Viral Replication by the Infectious Bronchitis Virus Endoribonuclease.Journal of virology · 2022Article
- The Multifunctional Faces of T-Cell Intracellular Antigen 1 in Health and Disease.International journal of molecular sciences · 2022Review
- Critical Roles of G3BP1 in Red-Spotted Grouper Nervous Necrosis Virus-Induced Stress Granule Formation and Viral Replication in Orange-Spotted Grouper (Frontiers in immunology · 2022Article
- Host Defence RNases as Antiviral Agents against Enveloped Single Stranded RNA Viruses.Virulence · 2021Review
- The Emerging Role of Stress Granules in Hepatocellular Carcinoma.International journal of molecular sciences · 2021Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Stress granules (SGs) are cytoplasmic structures that are induced in response to environmental stress, including viral infections. Here we report that hepatitis C virus (HCV) triggers the appearance of SGs in a PKR- and interferon (IFN)-dependent manner. Moreover, we show an inverse correlation between the presence of stress granules and the induction of IFN-stimulated proteins, i.e., MxA and USP18, in HCV-infected cells despite high-level expression of the corresponding MxA and USP18 mRNAs, suggesting that interferon-stimulated gene translation is inhibited in stress granule-containing HCV-infected cells. Finally, in short hairpin RNA (shRNA) knockdown experiments, we found that the stress granule proteins T-cell-restricted intracellular antigen 1 (TIA-1), TIA1-related protein (TIAR), and RasGAP-SH3 domain binding protein 1 (G3BP1) are required for efficient HCV RNA and protein accumulation at early time points in the infection and that G3BP1 and TIA-1 are required for intracellular and extracellular infectious virus production late in the infection, suggesting that they are required for virus assembly. In contrast, TIAR downregulation decreases extracellular infectious virus titers with little effect on intracellular RNA content or infectivity late in the infection, suggesting that it is required for infectious particle release. Collectively, these results illustrate that HCV exploits the stress granule machinery at least two ways: by inducing the formation of SGs by triggering PKR phosphorylation, thereby downregulating the translation of antiviral interferon-stimulated genes, and by co-opting SG proteins for its replication, assembly, and egress.
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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.