UBC Scientists Find Smoking Increases The Risk Of COVID-19
The studies of researchers from the University of British Columbia found that individuals with chronic obstructive pulmonary disease (COPD), or current cigarette smokers can have severe COVID-19 disease from SARS-CoV-2 infection. The above-mentioned individuals have high levels of angiotensin-converting enzyme II (ACE-2), which acts as the receptor for SARS-CoV-2 to invade the host cells. But the study says former smokers are safe as they have the same level of ACE II as those who never smoked.
The research findings suggest that you better quit smoking now to protect yourself from the deadly COVID-19. And COPD patients should strictly maintain social distancing and hygiene to prevent infection. The paper titled “ACE-2 Expression in the Small Airway Epithelia of Smokers and COPD Patients: Implications for COVID-19” got published in the European Respiratory Journal.
ACE-2, present in human cells, is the cellular entry receptor for the SARS-CoV-2 virus. To date, most of the severe COVID-19 cases have been in aged people who are above 55 years and with significant health conditions like COPD, while the virus infects individuals of any age group.
Janice Leung, Ph.D., who led the research, noted that patients with COPD
were at high risk for having severe COVID-19 in China. But the reason why most deaths occur in patients with chronic diseases like cardiovascular and Lung diseases is still unknown. The team hypothesized that the levels of ACE-2 could be higher in the airways of those people compared to people with no COPD.To study the hypothesis, they studied bronchial epithelial cells of lower respiratory tract collected from the lungs of 21 COPD patients and 21 individuals without COPD for ACE-2 expression. They also considered factors like if the samples are from individuals who never smoked, current smokers or former smokers.
They observed higher ACE-2 levels in the epithelial cells of current smokers and COPD patients. The ACE-2 levels were significantly higher in current smokers compared to those who never smoked. The findings were confirmed when they analyzed the data from two existing study groups that include 249 people—some former smokers, some current smokers, and some non-smokers.
This is the first study that demonstrates the increased ACE-2 expression in the airways of COPD patients and current smokers. The observations from previous studies in small animals were consistent with the new study.
The upregulation of ACE-2 might be helpful in protecting the host against lung injury but could turn out to be a disadvantage during COVID-19 infection as the virus uses it for its entry to cells.
The paper concluded, saying it highlights the importance of quitting smoking and prevention and rapid diagnosis in current smokers and COPD patients against the COVID-19 disease, as smoking and COPD increase the risk of COVID-19.
But the possibility of manipulating ACE-2 levels to improve the survival of COVID-19 patients is not discussed in the study.
