Importantly, low micromolar concentrations of cyclosporin A (<35 µM) substantially impacted the replication of SARS-CoV, human coronavirus 229E, and mouse hepatitis virus in cell culture. Cyclosporin A significantly inhibited gene expression and reduced progeny titers. Cyclosporin A treatment completely blocked SARS-CoV RNA and protein synthesis [196]. Cyclosporine A also in vitro reduced the replication of MERS-CoV, transmissible gastroenteritis coronavirus, porcine epidemic diarrhea virus, and feline coronavirus [196]. In fact, cyclosporine A has demonstrated broad-spectrum antiviral effects. It inhibited the replication of HBV, HCV, and HIV [197]. Cyclosporine also inhibited the replication of Zika virus, West Nile virus, Rift Valley fever virus, and influenza A virus by blocking the interaction of cellular cyclophilins with viral proteins as well as by inhibiting the RNA synthesis [198]. By targeting cyclophilins, the drug can also prevent acute lung injury [199]. Currently, the use of cyclosporin A is being tested in patients with moderate COVID-19 (NCT04412785; n = 20), hospitalized COVID-19 patients (NCT04392531; n = 120), and combined with topical corticosteroid in COVID-19 patients with acute keratoconjunctivitis (NCT04451239; n = 12). It has also been used in psoriatic COVID-19 patients [200].