Inflammation related to COVID-19 further increases oxidative stress, while oxidative stress, in turn, can promote inflammation. A basal redox regulation deficit thus might increase the risk to get trapped in this detrimental feedforward loop. Oxidative stress furthermore leads to oxidized phospholipids, commonly present in COVID-19 patient lungs. Oxidized phospholipids have been linked to coagulation abnormalities and low platelet counts, which are associated with adverse outcome of COVID-19 (Merad and Martin, 2020). Given that COVID-19 risk factors/conditions are commonly characterized by high oxidative stress levels it seems plausible that redox balance deficits are among the underlying mechanisms of vulnerability to COVID-19. Therefore, the potentially altered oxidative stress status linked to prematurity must be considered as it might exacerbate the clinical status.