ArticleJournal of virology2019
COPII Vesicle Transport Is Required for Rotavirus NSP4 Interaction with the Autophagy Protein LC3 II and Trafficking to Viroplasms.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- High-throughput quantitation of pathogen-induced calcium signals captured through live-cell fluorescence microscopy.Cell calcium · 2026Article
- Review
- Porcine Rotavirus NSP4 Inhibits Type I Interferon Production via NRBF2-Mediated Autophagic Degradation of MDA-5.Transboundary and emerging diseases · 2026Article
- Autophagy in emerging and highly concerned severe zoonotic infectious diseases.Frontiers in immunology · 2026Review
- Genome-wide CRISPR Screen Identifies Sec31A as a Key Regulator of Alpha Cell Survival.Nature communications · 2025Article
- Viroporin activity is necessary for intercellular calcium signals that contribute to viral pathogenesis.Science advances · 2025Article
- Virus infection and vesicle trafficking.Frontiers in immunology · 2025Review
- Duck STING mediates antiviral autophagy directing the interferon signaling pathway to inhibit duck plague virus infection.Veterinary research · 2024Article
- The protective role of prebiotics and probiotics on diarrhea and gut damage in the rotavirus-infected piglets.Journal of animal science and biotechnology · 2024Review
- Retinoic acid alleviates rotavirus-induced intestinal damage by regulating redox homeostasis and autophagic flux in piglets.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Article
- Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024Review
- Live Calcium Imaging of Virus-Infected Human Intestinal Organoid Monolayers Using Genetically Encoded Calcium Indicators.Journal of visualized experiments : JoVE · 2024Article
- Host IPmBio · 2024Article
- HDAC-Specific Inhibitors Induce the Release of Porcine Epidemic Diarrhea Virus via the COPII-Coated Vesicles.Viruses · 2023Article
- Review
- Article
- Re-Examining Rotavirus Innate Immune Evasion: Potential Applications of the Reverse Genetics System.mBio · 2022Review
- Rotavirus-Induced Lipid Droplet Biogenesis Is Critical for Virus Replication.Frontiers in physiology · 2022Review
- Sneaking into the viral safe-houses: Implications of host components in regulating integrity and dynamics of rotaviral replication factories.Frontiers in cellular and infection microbiology · 2022Review
- Functions of Viroporins in the Viral Life Cycle and Their Regulation of Host Cell Responses.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Many viruses that replicate in the cytoplasm dramatically remodel and stimulate the accumulation of host cell membranes for efficient replication by poorly understood mechanisms. For rotavirus, a critical step in virion assembly requires the accumulation of membranes adjacent to virus replication centers called viroplasms. Early electron microscopy studies describe viroplasm-associated membranes as "swollen" endoplasmic reticulum (ER). We previously demonstrated that rotavirus infection initiates cellular autophagy and that membranes containing the autophagy marker protein LC3 and the rotavirus ER-synthesized transmembrane glycoprotein NSP4 traffic to viroplasms, suggesting that NSP4 must exit the ER. This study aimed to address the mechanism of NSP4 exit from the ER and determine whether the viroplasm-associated membranes are ER derived. We report that (i) NSP4 exits the ER in COPII vesicles, resulting in disrupted COPII vesicle transport and ER exit sites; (ii) COPII vesicles are hijacked by LC3 II, which interacts with NSP4; and (iii) NSP4/LC3 II-containing membranes accumulate adjacent to viroplasms. In addition, the ER transmembrane proteins SERCA and calnexin were not detected in viroplasm-associated membranes, providing evidence that the rotavirus maturation process of "budding" occurs through autophagy-hijacked COPII vesicle membranes. These findings reveal a new mechanism for rotavirus maturation dependent on intracellular host protein transport and autophagy for the accumulation of membranes required for virus replication.
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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.