SARS-CoV-2 mortality in blacks and temperature-sensitivity to an angiotensin-2 receptor blocker

Forsdyke, Donald R.

Tropical climates provoke adaptations in skin pigmentation and in mechanisms controlling volume, salt-content and pressure of body fluids. For many whose distant ancestors moved to temperate climes, these adaptations proved harmful: pigmentation decreased by natural selection and susceptibility to hypertension emerged. Now an added risk is lung inflammation from coronavirus. Hypertension and coronavirus have in common angiotensin converting enzyme 2 (ACE2), which decreases blood pressure and mediates virus entry. In keeping with less detailed studies, a long-term case-report shows that decreased blood pressure induced by blocking a primary angiotensin receptor is supplemented, above critical blocker dosage, by a further temperature-dependent fall, likely mediated by ACE2 and a secondary angiotensin receptor. Temperature-dependence suggests a linkage with tropical heritage and an influence of blockers on the progress of coronavirus infections. Positive therapeutic results should result from negation of host pro-inflammatory effects mediated by the primary angiotensin receptor, and promotion of countervailing anti-inflammatory effects mediated by ACE2 through other receptors. Black vulnerability is likely based on physiological, not sociological, differences, which should guide treatment.