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 lungsbut 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.
The fatality rate of Covid-19 escalates with age and is larger in men than women. I show that these variations correlate strongly with the level of the viral receptor protein ACE2 in rat lungs, which is consistent with the still limited and apparently contradictory data on human ACE2. Surprisingly, lower levels of the receptor correlate with higher fatality. However, a previous mathematical model predicts that the speed of viral progression in URLanism has a maximum and then declines with the receptor level. Moreover, many manifestations of severe CoViD-19, such as severe lung injury, exacerbated inflammatory response and thrombotic problems may derive from increased Angiotensin II (Ang-II) level that results from degradation of ACE2 by the virus. I present here a mathematical model based on the influence of ACE2 on viral propagation and disease severity . The model fits Covid-19 fatality rate across age and sex with high accuracy (r^2>0.9) under the hypothesis that SARS-CoV-2 infections are in the dynamical regimes in which increased receptor slows down viral propagation. Moreover, rescaling the model parameters by the ratio of 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 sex, thus linking the molecular and epidemiological levels. The presented model opposes the fear that angiotensin receptor blockers (ARB), suggested as a therapy against the most adverse effects of CoViD-19 , may favour viral propagation, and suggests that Ang-II and ACE2 are candidate prognostic factors for detecting population that needs stronger protection.
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