ArticleNature communications2025
SARS-CoV-2 ORF3a drives dynamic dense body formation for optimal viral infectivity.
Article in Nature communications, 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.
- Circulating cholesterol fuels SARS-CoV-2 replication via ORF3a.EMBO reports · 2026Article
- SARS-CoV-2 Delta variant-specific ORF3a mutations destabilize lysosomal homeostasis to trigger lysosomal damage-mediated cell death.Communications biology · 2026Article
- ZDHHC18-Mediated Palmitoylation of ORF3a Promotes SARS-CoV-2 Pathogenesis by Antagonizing TRIM16-Mediated Ubiquitination and Proteasomal Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- A cocktail of SARS-CoV-2 S stem helix domain and receptor binding domain human monoclonal antibodies prevents the emergence of viral escape mutants.Microbiology spectrum · 2026Article
- BST-2 inhibits SARS-CoV-2 egress at intracellular membranes and is neutralized by ORF7a.Scientific reports · 2026Article
- Sensing the spectrum: diverse stimuli for the NLRP3 inflammasome.Communications biology · 2026Review
- Distinct virus-derived circular RNA molecule influences host response during SARS-CoV-2 infection.bioRxiv : the preprint server for biology · 2026Article
- SARS-CoV-2 Orf3a protein interaction mapping using unnatural amino acid incorporation.Protein engineering, design & selection : PEDS · 2026Article
- Computational modelling of the equine arteritis virus GP5/M Dimer: Implications for immune evasion and virulence.PloS one · 2026Article
- A cocktail of SARS-CoV-2 spike stem helix domain and receptor binding domain human monoclonal antibodies prevent the emerge of viral escape mutants.bioRxiv : the preprint server for biology · 2025Article
- What Has SARS-CoV-2 Taught Us About Evolution?Cureus · 2025Review
- Type A cholesterol-dependent cytolysins translocate to the trans-Golgi network for NLRP3 inflammasome activation.Nature immunology · 2025Article
- Bacterial toxins rewire the trans-Golgi network to activate the inflammatory response.Nature immunology · 2025Article
- A luminescent attenuated SARS-CoV-2 for the identification and validation of drug-resistant mutants.Journal of virology · 2025Article
- Hidden players of COVID-19: the evolving roles of SARS-CoV-2 accessory proteins.Frontiers in immunology · 2025Review
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5 authors.
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Abstract
SARS-CoV-2 hijacks multiple organelles for virion assembly, of which the mechanisms have not been fully understood. Here, we identified a SARS-CoV-2-driven membrane structure named the 3a dense body (3DB). 3DBs are unusual electron-dense and dynamic structures driven by the accessory protein ORF3a via remodeling a specific subset of the trans-Golgi network (TGN) and early endosomal membrane. 3DB formation is conserved in related bat and pangolin coronaviruses but was lost during the evolution to SARS-CoV. During SARS-CoV-2 infection, 3DB recruits the viral structural proteins spike (S) and membrane (M) and undergoes dynamic fusion/fission to maintain the optimal unprocessed-to-processed ratio of S on assembled virions. Disruption of 3DB formation resulted in virions assembled with an abnormal S processing rate, leading to a dramatic reduction in viral entry efficiency. Our study uncovers the crucial role of 3DB in maintaining maximal SARS-CoV-2 infectivity and highlights its potential as a target for COVID-19 prophylactics and therapeutics.
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