Does the pathogenesis of SARS-CoV-2 virus decrease at high-altitude?
AuthorArias-Reyes, C; Zubieta-DeUrioste, N; Poma-Machicao, L; Aliaga-Raudan, F; Carvajal-Rodriguez, F; Dutschmann, M; Schneider-Gasser, E; Zubieta-Calleja, G; Soliz, J
Source TitleRespiratory Physiology and Neurobiology
University of Melbourne Author/sDutschmann, Mathias
AffiliationFlorey Department of Neuroscience and Mental Health
Document TypeJournal Article
CitationsArias-Reyes, C., Zubieta-DeUrioste, N., Poma-Machicao, L., Aliaga-Raudan, F., Carvajal-Rodriguez, F., Dutschmann, M., Schneider-Gasser, E., Zubieta-Calleja, G. & Soliz, J. (2020). Does the pathogenesis of SARS-CoV-2 virus decrease at high-altitude?. RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY, 277, https://doi.org/10.1016/j.resp.2020.103443.
Access StatusAccess this item via the Open Access location
Open Access URLhttps://europepmc.org/articles/PMC7175867?pdf=render
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.
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