tacrolimus and Severe-Acute-Respiratory-Syndrome

Recent research has shown that Coronavirus (CoV) replication depends on active immunophilin pathways. Here we demonstrate that the drug FK506 (Tacrolimus) inhibited strongly the growth of human coronaviruses SARS-CoV, HCoV-NL63 and HCoV-229E at low, non-cytotoxic concentrations in cell culture. As shown by plaque titration, qPCR, Luciferase- and green fluorescent protein (GFP) reporter gene expression, replication was diminished by several orders of magnitude. Knockdown of the cellular FK506-binding proteins FKBP1A and FKBP1B in CaCo2 cells prevented replication of HCoV-NL63, suggesting the requirement of these members of the immunophilin family for virus growth.

Topics: Caco-2 Cells; Coronavirus 229E, Human; Coronavirus Infections; Coronavirus NL63, Human; Humans; Severe Acute Respiratory Syndrome; Severe acute respiratory syndrome-related coronavirus; Tacrolimus; Tacrolimus Binding Proteins; Virus Replication