STAT1 and acute respiratory distress syndrome: Then, the virus inhibits STAT-1 [18] phosphorylation to interfere with IFN-1 signalling; the third defensive mechanism is the exaggerated and prolonged production of IFN-1 by plasmacytoid dendritic cells (pDCs) to cause exhaustion so that the influx of inflammatory macrophages/monocytes and activated neutrophils occurs, resulting in pulmonary immunopathology such as acute respiratory distress syndrome (ARDS) [19].