ArticleCell research2021
SARS-CoV-2 envelope protein causes acute respiratory distress syndrome (ARDS)-like pathological damages and constitutes an antiviral target.
Article in Cell research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 1 of them a synthesis that pooled it.
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Who cites it
120 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Acute respiratory distress syndrome: potential of therapeutic interventions effective in treating progression from COVID-19 to treat progression from other illnesses-a systematic review.BMJ open respiratory research · 2023Pooled it
- Review
- SARS-CoV-2 E protein induces rapid TLR2-mediated T cell activation in mouse lungs revealed by intravital lung microscopy.The European respiratory journal · 2026Article
- Cleavage of TOM1 by the SARS-CoV-2 main protease NSP5 prevents autophagic degradation of viral envelope.Journal of virology · 2026Article
- SARS-CoV-2 envelope protein mitochondrial localization reveals host metabolic disruption.The Journal of biological chemistry · 2026Article
- SARS-CoV-2 nonspike structural proteins hijack mucosa epithelial cell fate.Cell death & disease · 2026Article
- Treating acute respiratory distress syndrome with a multifaceted nanomedicine: Inhibition of PANoptosis and enhancement of lung barrier integrity.Materials today. Bio · 2026Article
- Conserved Transmembrane Asparagine Is Essential for the Ion-Conducting Structure and Dynamics of the SARS-CoV-2 Envelope Protein.Journal of the American Chemical Society · 2026Article
- AI-driven breakthroughs in ion channel drug discovery: the future is now.Acta pharmacologica Sinica · 2026Article
- Structural and Computational Insights into the Attenuated Innate Immune Recognition of the SARS-CoV-2 N15 Lineage, an Early-Pandemic Variant.Computational and structural biotechnology journal · 2026Article
- HTRF-based identification of small molecules targeting SARS-CoV-2 E protein interaction with ZO-1 PDZ2.Scientific reports · 2025Article
- Beyond the Spike Glycoprotein: Mutational Signatures in SARS-CoV-2 Structural Proteins.Infectious disease reports · 2025Article
- Post-Translational Modifications in Respiratory Virus Infection: Recent Insights into the Development of In Vitro Models.International journal of molecular sciences · 2025Review
- Isogenic induced-pluripotent-stem-cell-derived airway- and alveolus-on-chip models reveal specific innate immune responses.Nature biomedical engineering · 2025Article
- The B169L protein of African swine fever virus functions as a viroporin that activates the calcium-mediated inflammasome.PLoS pathogens · 2025Article
- The NSP5, ORF6 and NSP13 of SARS-CoV-2 Cooperate to Modulate Inflammatory Cell Death Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Transient receptor potential channels in viral infectious diseases: Biological characteristics and regulatory mechanisms.Journal of advanced research · 2025Review
- Viroporins: emerging viral infection mechanisms and therapeutic targets.Journal of virology · 2025Review
- Production of SARS-CoV-2 virus-like particles as a vaccine candidate in stable cell lines through inducible E and M protein expression.BMC biotechnology · 2025Article
- Ion channel structure and function of the MERS coronavirus E protein.Science advances · 2025Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
34 authors at 5 institutions in 3 countries.
Funding
Abstract
Cytokine storm and multi-organ failure are the main causes of SARS-CoV-2-related death. However, the origin of excessive damages caused by SARS-CoV-2 remains largely unknown. Here we show that the SARS-CoV-2 envelope (2-E) protein alone is able to cause acute respiratory distress syndrome (ARDS)-like damages in vitro and in vivo. 2-E proteins were found to form a type of pH-sensitive cation channels in bilayer lipid membranes. As observed in SARS-CoV-2-infected cells, heterologous expression of 2-E channels induced rapid cell death in various susceptible cell types and robust secretion of cytokines and chemokines in macrophages. Intravenous administration of purified 2-E protein into mice caused ARDS-like pathological damages in lung and spleen. A dominant negative mutation lowering 2-E channel activity attenuated cell death and SARS-CoV-2 production. Newly identified channel inhibitors exhibited potent anti-SARS-CoV-2 activity and excellent cell protective activity in vitro and these activities were positively correlated with inhibition of 2-E channel. Importantly, prophylactic and therapeutic administration of the channel inhibitor effectively reduced both the viral load and secretion of inflammation cytokines in lungs of SARS-CoV-2-infected transgenic mice expressing human angiotensin-converting enzyme 2 (hACE-2). Our study supports that 2-E is a promising drug target against SARS-CoV-2.
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