Scientists have recently discovered that those with allergic asthma—a condition in which the airways tighten due to inhaled allergens—may be less susceptible to the COVID-19 virus.
This has to do with their immune response. Studies have shown that the proteins that trigger excess mucus production and narrowing of airways in those with allergic asthma may form a shield around vulnerable respiratory cells, thereby protecting them from the virus. This finding explains why these patients are less susceptible to COVID-19 compared to those with other lung-related conditions.
What Is Asthma?
Asthma is a respiratory condition that causes inflammation in the lungs. Common symptoms include coughing, wheezing, chest tightness, and breathlessness. In the United States, it affects approximately 8 percent of the population, 60% of which have allergic asthma.
Unlike ‘regular’ asthma, which can be set off by exercise or weather, allergic asthma is triggered by an allergy. For example, it can be caused by pollen, pet dander, and dust mites.
In most cases, asthma is a risk factor when it comes to respiratory conditions such as colds and flus (those with asthma are at a higher risk of developing these viral infections). Researchers have also warned at the beginning of the pandemic that it may put people at a greater risk for severe COVID-19. The same goes for other lung disorders such as COPD.
As the pandemic progressed, however, they’ve noticed something interesting—those with allergic asthma did not develop severe COVID-19 like they thought they would. To find out why, they conducted a number of studies with airway-lining cells.
Protection from IL-13
Interleukin-13 (IL-13) sets allergic asthma apart from other types of asthma. Part of the inflammatory process, this protein usually helps the body fight off worms and other parties. In those with allergic asthma, however, the body mistakenly attacks pollen and other harmless substances as parasites.
However, it wasn’t clear to researchers how IL-13 protected them from the COVID-19 virus. To find out, they grew cells from the lining of the lungs from six donors, some of which were treated with the IL-13 protein to mimic allergic asthma. They then infected some of these cells with the virus.
They quickly discovered that the coronavirus preferred ciliated cells. Mucus-producing goblet cells, on the other hand, were rarely infected. They believe this is due to a protein called ACE2, which is prominent on the surface of ciliated cells (goblet cells do not have as many of these proteins). Ultimately, it’s this ACE2 protein that the coronavirus uses to enter cells.
When researchers doused the cells with the IL-13 protein, cilia beating on these cells decreased. This may prevent the coronavirus from spreading. Not only that, but it also triggered the airway-lining cells to release a type of sticky mucus, ones that are responsible for trapping viruses. Researchers believe that this extra mucus may help expel the virus from the lungs before they’re able to do significant damage.
That’s not all, they also found that IL-13 causes the respiratory cells to produce less ACE2, the protein that the virus uses as a gateway into cells. This makes it much harder for them to cause infection.
This may explain why those the allergic asthma are less susceptible to severe COVID-19. It’s important to note, however, that despite this extra protection, individuals can still get infected, and given the potential consequences (e.g. long COVID), it’s still highly recommended that you take precautionary measures. After all, it’s not a virus that you want to mess around with. Even if severe symptoms are rare, it’s not something that you want to put yourself at risk for.
