Does the pathogenesis of SARS-CoV-2 virus decrease at high-altitude?

Respir Physiol Neurobiol. 2020 Jun;277:103443. doi: 10.1016/j.resp.2020.103443. Epub 2020 Apr 22.

Abstract

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.

Keywords: COVID-19; Hypoxia; Lung remodeling; UV.

MeSH terms

  • Altitude
  • Betacoronavirus / pathogenicity
  • Betacoronavirus / physiology*
  • Bolivia / epidemiology
  • COVID-19
  • Coronavirus Infections / epidemiology*
  • Coronavirus Infections / virology*
  • Disease Susceptibility
  • Ecuador / epidemiology
  • Humans
  • Oxygen
  • Pandemics
  • Pneumonia, Viral / epidemiology*
  • Pneumonia, Viral / virology*
  • SARS-CoV-2
  • Tibet / epidemiology
  • Virulence

Substances

  • Oxygen