ArticlePLoS pathogens2018
Inclusion bodies of human parainfluenza virus type 3 inhibit antiviral stress granule formation by shielding viral RNAs.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- Host restriction factor SAMHD1 does not restrict seasonal influenza virus replication in human epithelial or macrophage-like cells.Virology journal · 2026Article
- Host factors in parainfluenza virus replication: from entry to innate immunity evasion.Frontiers in immunology · 2026Review
- Prediction of Small-Molecule Partitioning into Biomolecular Condensates from Simulation.JACS Au · 2025Article
- Stress granules and cell death: crosstalk and potential therapeutic strategies in infectious diseases.Cell death & disease · 2025Review
- Multi-Faceted Roles of Stress Granules in Viral Infection.Microorganisms · 2025Review
- Prediction of small-molecule partitioning into biomolecular condensates from simulation.bioRxiv : the preprint server for biology · 2025Article
- Modeling biomolecular condensates across scales: Atomistic, coarse-grained, and data-driven approaches.Advances in physics: X · 2025Article
- Non-Structural Protein V of Canine Distemper Virus Induces Autophagy via PI3K/AKT/mTOR Pathway to Facilitate Viral Replication.International journal of molecular sciences · 2024Article
- Critical role of G3BP1 in bovine parainfluenza virus type 3 (BPIV3)-inhibition of stress granules formation and viral replication.Frontiers in immunology · 2024Article
- Immunoinformatics-aided rational design of multiepitope-based peptide vaccine (MEBV) targeting human parainfluenza virus 3 (HPIV-3) stable proteins.Journal, genetic engineering & biotechnology · 2023Article
- Spatial and functional arrangement of Ebola virus polymerase inside phase-separated viral factories.Nature communications · 2023Article
- A little less aggregation a little more replication: Viral manipulation of stress granules.Wiley interdisciplinary reviews. RNA · 2023Review
- Vimentin inhibits α-tubulin acetylation via enhancing α-TAT1 degradation to suppress the replication of human parainfluenza virus type 3.PLoS pathogens · 2022Article
- Insights into the SARS-CoV-2-Mediated Alteration in the Stress Granule Protein Regulatory Networks in Humans.Pathogens (Basel, Switzerland) · 2021Article
- Human Parainfluenza Virus 3 Phosphoprotein Is a Tetramer and Shares Structural and Interaction Features with Ebola Phosphoprotein VP35.Biomolecules · 2021Article
- Identification of a Region in the Common Amino-terminal Domain of Hendra Virus P, V, and W Proteins Responsible for Phase Transition and Amyloid Formation.Biomolecules · 2021Article
- SARS-CoV-2 nucleocapsid protein phase separates with G3BPs to disassemble stress granules and facilitate viral production.Science bulletin · 2021Article
- SARS-CoV-2 nucleocapsid protein impairs stress granule formation to promote viral replication.Cell discovery · 2021Article
- Oxidative stress-induced mitophagy is suppressed by the miR-106b-93-25 cluster in a protective manner.Cell death & disease · 2021Article
- Evasion of Host Antiviral Innate Immunity by Paramyxovirus Accessory Proteins.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral invasion triggers the activation of the host antiviral response. Besides the innate immune response, stress granules (SGs) also act as an additional defense response to combat viral replication. However, many viruses have evolved various strategies to suppress SG formation to facilitate their own replication. Here, we show that viral mRNAs derived from human parainfluenza virus type 3 (HPIV3) infection induce SG formation in an eIF2α phosphorylation- and PKR-dependent manner in which viral mRNAs are sequestered and viral replication is inhibited independent of the interferon signaling pathway. Furthermore, we found that inclusion body (IB) formation by the interaction of the nucleoprotein (N) and phosphoprotein (P) of HPIV3 correlated with SG suppression. In addition, co-expression of P with NL478A (a point mutant of N, which is unable to form IBs with P) or with NΔN10 (lacking N-terminal 10 amino acids of N, which could form IBs with P but was unable to synthesize or shield viral RNAs) failed to inhibit SG formation, suggesting that inhibition of SG formation also correlates with the capacity of IBs to synthesize and shield viral RNAs. Therefore, we provide a model whereby viral IBs escape the antiviral effect of SGs by concealing their own newly synthesized viral RNAs and offer new insights into the emerging role of IBs in viral replication.
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