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 problemsand exacerbates the inflammatory responsedue 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.
The fatality rate of SARS-Cov-2 escalates with age and is larger in men than women. I show that these variations are strongly correlated with the levels of the ACE2 protein in the lungs but surprisingly , despite ACE2 is the viral receptor, higher levels lead to lower fatality. This behaviour is consistent with a previous mathematical model that predicts that the speed of viral progression in URLanism has a maximum and then declines with the receptor level. SARS-Cov-2 degrades ACE2 and thus worsens lung injury, causes vasoconstriction, thrombotic problems, and exacerbated inflammatory response. I developed a mathematical model based on the influence of ACE2 on 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). Rescaling the model parameters with the binding rates of the spike proteins of SARS-CoV and SARS-CoV-2 allows predicting the fatality rate of SARS-CoV across age and gender , in particular its higher severity for young patients , thus linking the molecular and epidemiological levels. These results support the suggestion that drugs that enhance the expression of ACE2 , such as ACE inhibitors and angiotensin receptor blockers, constitute a promising therapy against the most adverse effects of CoViD-19 . Furthermore, ACE2 is a candidate prognostic factor for detecting population that needs stronger protection.
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