There are striking differences in the lethality of the Covid-19 disease, from more than 90\% estimated infected persons that experience only very weak or no symptoms to cases that require ICU assistance and result in death. The fatality rate escalates dramatically with age and is much larger in males than in females . I show here these dramatic variations in fatality rates across age and gender are impressively strongly correlated (r^2=0.91 with only one free parameter) with levels of the ACE2 protein in rat lungs, which are in turn qualitatively similar to expression in humans . This behaviour is predicted by a model that assumes that deaths are caused by the degradation of the ACE2 receptor by the virus , which uses it as entry point in the cells. The insufficient levelof ACE2 exacerbates the inflammatory response eventually leading to death, but if the initial levels of ACE2 are high the immune system has enough time to resolve the infection before it gets to extreme consequences. These results are consistent with previous hypothesis on the protective role of ACE2, and suggest that , counterintuitively, drugs that act synergistically with ACE2 and enhance its expression, such as ACE inhibitors and angiotensin receptor blockers used to treat high blood pressure, may offer a promising therapy against the most adverse effects of the Covid-19 disease. ACE2 is also candidate to be a prognostic factor and a risk factor for detecting population that needs stronger protection.
 The fatality rate of SARS-Cov-2 escalates with age and is larger in men than women . I show that these variations across age and gender are quantitatively explained by the levels of the ACE2 protein in the lungs. This correlation also rationalizes the association between Covid-19 lethality and hypertension. Surprisingly, despite ACE2 is the viral receptor, higher values of ACE2 lead to lower fatality . This behaviour is consistent with a previous mathematical model that predicts that the speed of the virus in URLanism has a maximum and then declines with receptor level. SARS-Cov-2 degrades ACE2 and thus worsens lung injury, causes vasoconstriction, possible thrombotic problems and exacerbates the inflammatory response due to the cross-talk between ACE2, the prothrombotic state and the immune system. I develop here a mathematical model based on the influence of ACE2 on the speed of viral propagation and on the negative effects of its degradation. The model fits SARS-CoV-2 fatality rate across age and gender with high accuracy (r^2~0.9). Strikingly, rescaling the fitted models with the binding rates of the spike proteins of SARS and SARS-CoV-2 allow predicting the fatality rate of SARS across age and gender with high accuracy, in particular its higher severity for young patients. The epidemiology of the common-cold coronavirus NL63 is also consistent with the model and existing data on the affinity of its spike protein, thus linking the molecular and epidemiological levels. These results support the suggestion that drugs that act synergistically with ACE2 and enhance its expression, such as ACE inhibitors and angiotensin receptor blockers , may constitute a promising therapy against the most adverse effects of CoViD-19, including hyperinflammation and thrombotic complications. Furthermore, ACE2 is a candidate prognostic factor for detecting population that needs stronger protection.
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