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An article revealed in Frontiers in Physiology tends to point out that populations residing above 2500 meters are much less vulnerable to Covid-19. Adaptation to oxygen deprivation would cut back SARS-CoV-2 an infection by a posh mechanism involving the renin-angiotensin system that Jean-Marc Sabatier has typically described right here.

This can be a very technical article by Christian Devaux and Didier Raoult revealed on August 25, 2022 in the scientific journal Frontiers in Physiology. The 2 well-known professors observe that an epidemiological report carried out amongst populations residing on the Andean Altiplano in South America (Peru and Bolivia), on the Tibetan plateaus in Asia and on the Ethiopian excessive plateaus in Africa, thus above 2500 meters of altitude, have been much less involved by the SARS-CoV-2 an infection. The speculation put ahead can be an adaptation to hypoxia, the dearth of oxygen provide to the physique’s tissues. It stays to be understood what the mechanisms are.

The RAS hormonal system

The 2 authors of the article set up the direct hyperlink between hypoxia and the over-activation of the AT1R receptor of the renin-angiotensin system (RAS). This ubiquitous hormonal system within the physique controls all organs and tissues in our physique.
On this paper, hypoxia would cut back the flexibility of SARS-CoV-2 to bind and enter goal cells, conversely activation of HIF-1α (the hypoxia-induced issue) might cut back antiviral immune defenses and exacerbate pro-inflammatory responses and thrombosis which can be detrimental to SARS-CoV-2 contaminated people.
Now, Covid-19 attributable to SARS-CoV-2 that emerged in China in November 2019 is primarily characterised by acute respiratory misery, a storm of pro-inflammatory cytokines, and thrombotic occasions resulting in a number of important organ dysfunctions that may result in loss of life.
“At 4,000 m altitude, every breath of air incorporates solely 60% of the oxygen molecules current in the identical breath at sea degree. Adaptation to hypoxia happens by air flow, which controls the quantity of air and oxygen delivered to the pulmonary alveoli and results in the next focus of erythrocyte (pink blood cell) hemoglobin within the bloodstream that picks up oxygen exchanged by the alveolar-capillary system.”
Thus the renin-angiotensin system (RAS) pathway in high-altitude populations and its imbalance in coronavirus illness appears as soon as once more confirmed.

The goal of the virus

For 2 and a half years now, Jean-Marc Sabatier* has been asserting that Covid-19 ailments are attributable to an over-activation of the AT1R receptor of the RAS. This over-activation is because of an extra of angiotensin 2, insufficiently degraded by the ACE2 receptor which is the goal of the virus.

In keeping with Jean-Marc Sabatier, in disagreement with what’s described within the Frontiers in Physiology article, it’s the over-activated AT1R receptor that’s instantly accountable for hypoxia (hypoxic stress), along with its different deleterious actions. The activation of the hypoxia-induced issue is just a response of the organism to hypoxic stress, with none direct hyperlink with a discount of anti-viral immune defenses and exacerbation of pro-inflammatory and pro-thrombotic responses.
It must be remembered that the AT1R receptor has pro-hypertensive, pro-inflammatory, pro-oxidant, pro-angiogenic, pro-fibrosing, pro-thrombotic and pro-hypertrophying actions. Whereas inhibiting the manufacturing of nitric oxide (NO) concerned in inflammatory, immune and reminiscence phenomena.

*Jean-Marc Sabatier is Director of Analysis on the CNRS and holds a PhD in Cell Biology and Microbiology and an HDR in Biochemistry. Editor-in-Chief of the worldwide scientific journals: “Coronaviruses” and “Infectious Issues – Drug Targets”. He’s talking in his personal identify.

And if the “SRA” defined the Covid-19?