Thus, a model for the triggering mechanism of ARDS and associated cardio-respiratory instability in the hyper acute cases of COVID-19 would be direct involvement of the virus causing decreased ACE2 availability and subsequent reduction on BK degradation via spike protein-dependent interactions, leading to increased downstream BK signaling in the endothelial cells via BKRB2, alveolar capillary leak, and infiltration of activated immune cells (43). This evidence concerns the gene CHMP5 and acute respiratory distress syndrome.