April 2023 Br J Cardiol 2023;30:75–6 doi:10.5837/bjc.2023.011
Artemio García-Escobar, Silvio Vera-Vera, Daniel Tébar-Márquez, Alfonso Jurado-Román, Santiago Jiménez-Valero, Guillermo Galeote, José Ángel Cabrera, Raul Moreno
Introduction Retrospective studies revealed that vitamin D may protect against severe COVID-19 disease,1,2 and some pilot studies suggest that it even improves prognosis.3,4 The two most widely accepted theories are the vitamin D modulation of immunity and the renin–angiotensin system.5,6 So far, the mechanism of the benefit of vitamin D in COVID-19 remains unknown. Role of ACE2 Angiotensin-converting enzyme 2 (ACE2) converts angiotensin (Ang) II to Ang(1–7) and Ang I to Ang(1–9) (figure 1).7 Ang(1–7) has a very short half-life (<9 seconds), and the release of a soluble catalytic ectodomain of ACE2 (ceACE2) from the vascular endoth
June 2020 Br J Cardiol 2020;27:55–9 doi:10.5837/bjc.2020.018
Cormac T O’Connor, David Mulcahy
The virology of COVID-19 The COVID-19 virus shares the majority of its genome with a previously identified bat coronavirus species RaTG13.3,4 In a fashion similar to the SARS coronavirus from 2002/2003, COVID-19 enters the cell when its ‘spike protein’ interacts with the ACE2 protein in host cells, and allows passage into the cell (see figure 1). Though COVID-19 is, on the whole, most identifiable with the bat coronavirus RaTG13, the spike protein on its own is more akin to that seen in coronavirus species seen in the Malayan pangolin.4 The spike protein in the COVID-19 virus was found to have similar (albeit less) binding affinity for th
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