People with chronic obstructive pulmonary disease (COPD) and people who currently smoke may have higher levels of a molecule, called angiotensin converting enzyme II (ACE-2), in their lungs according to a study published in the European Respiratory Journal (ERJ).
Previous research shows that ACE-2, which sits on the surface of lung cells, is the ‘entry point’ that allows coronavirus to get into the cells of the lungs and cause an infection.
The new study also shows that levels of ACE-2 in former smokers is lower than in current smokers.
The research was led by Dr Janice Leung at the University of British Columbia and St. Paul’s Hospital, Vancouver, Canada. She said: “The data emerging from China suggested that patients with COPD were at higher risk of having worse outcomes from COVID-19. We hypothesised that this could be because the levels of ACE-2 in their airways might be increased compared to people without COPD, which could possibly make it easier for the virus to infect the airway.”
Read more at European Lung Foundation
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