“…Although subjects suffering from COVID-19 are at increased risk of thrombosis, and we have strong evidence that subjects with HHT often suffer from medical conditions that may negatively influence the clinical course of COVID-19 (like chronic anemia, heart failure, and pulmonary AVMs), recent data suggest that, actually, HHT patients may generally present milder forms of SARS-CoV2 infection [ 70 , 71 , 72 , 73 , 74 , 75 , 76 ]. Some preliminary data show a significant decrease in inflammatory cytokines detected in the HHT population—with differences lower than 50% for some cytokines like interleukines (ILs: IL-6, IL-1β, and IL12p40) and around 50% for Chemokine (C-C motif) ligand 20 (CCL20), Thrombospondin-1 (TSP-1), and Activin A [ 70 , 71 , 72 , 73 , 74 , 75 , 76 ]. If confirmed by larger studies, these HHT characteristics may explain some sort of protection against developing severe forms of COVID-19 [ 70 , 71 , 72 , 73 ].…”