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dc.contributor.authorArias-Reyes, C
dc.contributor.authorZubieta-DeUrioste, N
dc.contributor.authorPoma-Machicao, L
dc.contributor.authorAliaga-Raudan, F
dc.contributor.authorCarvajal-Rodriguez, F
dc.contributor.authorDutschmann, M
dc.contributor.authorSchneider-Gasser, E
dc.contributor.authorZubieta-Calleja, G
dc.contributor.authorSoliz, J
dc.identifierpii: S1569-9048(20)30101-4
dc.identifier.citationArias-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,
dc.description.abstractIn 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.
dc.titleDoes the pathogenesis of SARS-CoV-2 virus decrease at high-altitude?
dc.typeJournal Article
melbourne.affiliation.departmentFlorey Department of Neuroscience and Mental Health
melbourne.source.titleRespiratory Physiology and Neurobiology
melbourne.contributor.authorDutschmann, Mathias
melbourne.accessrightsThis item is currently not available from this repository

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