Coronaviruses shares ACE2 functional receptors with human cardiovascular system.

What is it about?

As it was previously stated, for the establishment of SARS coronavirus infections, the endocytosis of virus particles into host cells is needed. Surprisingly, the ACE2 has been identified as a functional receptor,3 as ACE2–Spike interaction is the mechanisms that lead through a process of internalization with ACE2, to the endocytosis4. This mechanism is shared with all SARS coronavirus family that, now, includes the SARS‐CoV‐2 causing the severe COVID‐19.

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Why is it important?

How is common to share biomolecular targets between viruses and active mediators of the cardiovascular system? Is it a “coincidence” due to the spread over species and ancient phylogeny of renin–angiotensin system? I mean, do viruses use as a binding site a functional receptor that is, usually, involved in the control of vascular tone, arterial blood pressure, and fibrotic response to damage? Is this functional? Or, instead, if this is not common, it is a possible evolution of viruses, eventually, driven by experiments and/or worldwide use of treatment targeting RAAS receptors? This fact raises questions on safety when using ACEi and angiotensin receptor blockers (ARBs) in patients affected by COVID‐19, as these therapies, which are widely used for the treatment of high blood pressure and heart failure, having as main target ACE1, can cause the upregulation of ACE2, with the consequence of open access routes to the COVID‐19. On the contrary, it is not possible to exclude that less‐selective ACEi/ARBs might be also helpful by blocking, even partially, ACE2. In this regard, it might be useful to obtain epidemiological data on patients affected by COVID‐19 that are assuming ACEi/ARB.