Ptarmigan wrote: ↑Tue Jun 02, 2020 8:51 pmDoes the pathogenesis of SAR-CoV-2 virus decrease at high-altitude?
Our epidemiological analysis of the Covid-19 pandemic clearly indicates a decrease of prevalence and impact of SARS-CoV-2 infection in populations living at altitude of above 3,000 masl. The reason for decreased severity of the global COVID-19 outbreak at high altitude could relate to both environmental and physiological factors.
Environmental factors may influence the virulence of SARS-CoV-2 at high-altitude. Indeed, a high-altitude environment is characterized by drastic changes in temperature between night and day, air dryness, and high levels of ultraviolet (UV) light radiation (United-States-Environmental-Protection-Agency 2017). In particular UV light radiation A (UVA) and B (UVB) is well known to be capable of producing alterations in the molecular bonds of the DNA and RNA, and thus UV radiation at high-altitude may act as a natural sanitizer (Andrade 2020; Zubieta-Calleja 2020a; Zubieta-Calleja and Zubieta-DeUrioste 2017). In relation to SARS-CoV-2, while complete disinfection cannot be achieved by UVA and UVB, these radiations should shorten the half-life of any given virus (Andrade 2020; Zubieta-Calleja 2020b). It is clear that, all together, these factors may dramatically reduce the “survival” capacity of the virus at high-altitude, and therefore its virulence. Finally, due to the lower density of air and greater distance between molecules at high-altitude, the size of the airborne virus inoculum must be smaller than at sea level.
Although the data of the present study suggest a strongly decreased pathogenicity of SARS-CoV-2 in high-altitude, there is yet no evidence of an underlying physiological mechanisms that could affect to severity of infection. However, there is a positive correlation between the infection rate of SARS-CoV-1 and ACE2 in pulmonary epithelial cells. Importantly both SARS-CoV-1 and SARS-CoV-2 bind to ACE2 (Lu et al. 2020; Rothan and Byrareddy 2020; van Doremalen et al., 2020), and thus a putative decrease of ACE2 expression in pulmonary endothelia in high-altitude inhabitant could represent a physiological protective for the severe and often lethal pulmonary edema.
Another factor is that people living at high altitude, especially those who are children of high altitude dwellers have adapted their lungs and pulmonary circulation and have a much higher capacity than se level resident. Their adaptations also make them less susceptible to lung edema.
Another consequence of increased HIF-1 at altitude is an increase in AMP kinase which can fight inflammation. Interesting news indeed!