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Does the pathogenesis of SARS-CoV-2 virus decrease at high-altitude?
Respiratory Physiology & Neurobiology ( IF 2.3 ) Pub Date : 2020-04-22 , DOI: 10.1016/j.resp.2020.103443 Christian Arias-Reyes 1 , Natalia Zubieta-DeUrioste 2 , Liliana Poma-Machicao 1 , Fernanda Aliaga-Raduan 1 , Favio Carvajal-Rodriguez 1 , Mathias Dutschmann 3 , Edith M Schneider-Gasser 4 , Gustavo Zubieta-Calleja 2 , Jorge Soliz 5
Respiratory Physiology & Neurobiology ( IF 2.3 ) Pub Date : 2020-04-22 , DOI: 10.1016/j.resp.2020.103443 Christian Arias-Reyes 1 , Natalia Zubieta-DeUrioste 2 , Liliana Poma-Machicao 1 , Fernanda Aliaga-Raduan 1 , Favio Carvajal-Rodriguez 1 , Mathias Dutschmann 3 , Edith M Schneider-Gasser 4 , Gustavo Zubieta-Calleja 2 , Jorge Soliz 5
Affiliation
In the present study we analyze the epidemiological data of COVID-19 of Tibet and high-altitude regions of Bolivia and Ecuador, and compare to lowland data, to test the hypothesis that high-altitude inhabitants (+2,500 m above sea-level) are less susceptible to develop severe adverse effects in acute SARS-CoV-2 virus infection. Analysis of available epidemiological data suggest that physiological acclimatization/adaptation that counterbalance the hypoxic environment in high-altitude may protect from severe impact of acute SARS-CoV-2 virus infection. Potential underlying mechanisms such as: (i) a compromised half-live of the virus caused by the high-altitude environment, and (ii) a hypoxia mediated down regulation of angiotensin-converting enzyme 2 (ACE2), which is the main binding target of SARS-CoV-2 virus in the pulmonary epithelium are discussed.
更新日期：2020-04-22
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