ArticlePLoS pathogens2025
SARS-CoV-2 remodels the Golgi apparatus to facilitate viral assembly and secretion.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Rab10 coordinates SADS-CoV non-lytic egress through the ERGIC-TGN-lysosome trafficking pathway.PLoS pathogens · 2026Article
- The ER-Golgi intermediate compartment: a central hub integrating membrane trafficking and stress responses.EMBO reports · 2026Review
- Super-resolution atlas of SARS-CoV-2 infection reveals protease-dependent organelle maturation, dsRNA landscapes, and intracellular structural proteins.Nature communications · 2026Article
- BST-2 inhibits SARS-CoV-2 egress at intracellular membranes and is neutralized by ORF7a.Scientific reports · 2026Article
- TMPRSS2-induced Golgi disruption restricts the incorporation of virus envelope glycoproteins into virions.EMBO reports · 2026Article
- Coronavirus M protein disperses the trans-Golgi network and inhibits anterograde protein trafficking in the secretory pathway.PLoS pathogens · 2026Article
- Distinct virus-derived circular RNA molecule influences host response during SARS-CoV-2 infection.bioRxiv : the preprint server for biology · 2026Article
- VPS26A retromer complex and SNX27 mediate stress-induced Golgi bypass of membrane proteins.Nature communications · 2026Article
- COVID-19 Prophylactic Effect of Bromhexine Hydrochloride.Immunity, inflammation and disease · 2026Article
- Protein Kinase D2 Regulates GRASP65 Phosphorylation and Golgi Ribbon Unlinking During G2/M Transition.Cells · 2026Article
- Molecular Aspects of Viral Pathogenesis in Emerging SARS-CoV-2 Variants: Evolving Mechanisms of Infection and Host Response.International journal of molecular sciences · 2026Review
- COP I vesicles facilitate classical swine fever virus proliferation by transporting fatty acid synthase from the Golgi apparatus to the endoplasmic reticulum.Journal of virology · 2025Article
- The SARS-CoV-2 envelope PDZ binding motif acts as a virulence factor disrupting host's epithelial cell-cell junctions.Cellular & molecular biology letters · 2025Article
- Genetic Analysis and Predictive Modeling of COVID-19 Severity in a Hospital-Based Patient Cohort.Biomolecules · 2025Article
- Lysosomes' fallback strategies: more than just survival or death.Frontiers in cell and developmental biology · 2025Review
- SARS-CoV-2 Assembly: Gaining Infectivity and Beyond.Viruses · 2024Review
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13 authors.
Funding
Abstract
The COVID-19 pandemic is caused by the enveloped virus SARS-CoV-2. Despite extensive investigation, the molecular mechanisms for its assembly and secretion remain largely elusive. Here, we show that SARS-CoV-2 infection induces global alterations of the host endomembrane system, including dramatic Golgi fragmentation. SARS-CoV-2 virions are enriched in the fragmented Golgi. Blocking endoplasmic reticulum (ER) to Golgi trafficking dramatically inhibits SARS-CoV-2 assembly and secretion without reducing viral genome replication. Significantly, SARS-CoV-2 infection down-regulates GRASP55 but up-regulates TGN46 protein levels. Surprisingly, GRASP55 expression reduces both viral secretion and spike number on each virion without affecting viral entry, while GRASP55 depletion displays opposite effects. In contrast, TGN46 depletion only inhibits viral secretion without affecting spike incorporation into virions. Taken together, we show that SARS-CoV-2 alters Golgi structure and function to modulate viral assembly and secretion, highlighting the Golgi as a potential therapeutic target for blocking SARS-CoV-2 infection.
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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.