SARS-CoV-2 Nucleocapsid Protein Triggers Hyperinflammation via Protein-Protein Interaction-Mediated Intracellular Cl⁻ Accumulation in Respiratory Epithelium

Using human respiratory epithelial cell lines, primary cultured human airway epithelial cells, and murine models of viral structural protein stimulation and SARS-CoV-2 direct challenge, scientists demonstrated that SARS-CoV-2 nucleocapsid protein could interact with Smad3, which downregulated cystic fibrosis transmembrane conductance regulator expression via microRNA-145.