Alu retrotransposons and COVID-19 susceptibility and morbidity

Figures

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  Fig. 1. Alu polymorphism within ACE intron 16 influences circulating ACE enzyme. ACE II, ID, and DD are three ACE genotypes generated by Alu insertion/deletion events. These genotypes affect the circulating level of ACE encoded by the gene. Specifically, individuals with the II genotype have the lowest circulating ACE levels whereas individuals having the DD genotype tend to have the highest-circulating ACE level. I, insertion; D, deletion

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  Fig. 2. The frequency of polymorphic Alu insertion in populations of different origin of genetic ancestry (OGA). OGAs are arranged to show an ascending frequency of Alu insertion in ACE for visualization purposes. ACE and F13B are similarly correlated with OGA, where it is the lowest in individuals with genetic ancestry associated with African populations and the highest in Asian populations. The Alu polymorphism in PLAT shares the trend with ACE and F13B but not as closely. The frequency of Alu insertion in PGR does not assume the increase observed with the polymorphisms in the other three genes. We recognize that genetic data have been misused to stigmatize ethnic groups or individuals and the usage of Alu frequencies reported herein for such purposes will not be tolerated ethically and is not scientifically justified

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  Fig. 3. SARS-CoV-2 and relevant biological processes that involve ACE, PGR, FXIIIB, and tPA. SARS-CoV-2 uses ACE2 as a receptor for cell entry, facilitated by androgen-regulated TMPRSS2. SARS-CoV-2 can cause tissue and endothelial cell damages, activating the intertwined intrinsic and extrinsic blood coagulation pathways. ACE and ACE2 are two essential regulatory components in the RAAS. ACE can promote vasoconstriction through antagonizing the regulatory role of ACE2 in the RAAS and acting as a bradykininase in the KKS additionally activated by the intrinsic coagulation pathway. ACE2 is locally downregulated by SARS-CoV-2 entry and excessive ACE signaling. Progesterone can upregulate ACE2 via binding to the intracellular progesterone receptor. The result of hemostasis is the conversion of fibrin monomers to polymers catalyzed by Factor XIII, which, in circulation, is a heterotetrameric protein composed of FXIIIA and FXIIIB subunits. D-dimers constitute one of the fibrinolysis degradation products generated as plasmin catalyzes fibrinolysis. Plasminogen is the zymogen of plasmin; the transition can be facilitated by kallikrein and tPA among other molecules. Both plasmin and FXIIIB can…