Some types of asthma protect against severe COVID-19, and we finally know why

(ORDO NEWS) — When the COVID-19 pandemic first began, people with chronic lung conditions such as asthma were worried that the illness would be particularly hard on them. However, as it turns out, people with some types of asthma do better than expected – and we can finally understand why.

Population-based studies in Australia, the UK, Europe and the US have so far found no evidence that asthma causes severe symptoms of COVID-19.

In fact, everything is just the opposite. In general, people with allergic asthma are less likely to get sick after being infected with SARS-CoV-2; unlike people with other lung conditions, such as emphysema, who are more likely to experience severe symptoms.

What distinguishes patients with asthma? Researchers at the University of North Carolina at Chapel Hill think they’ve finally figured it out.

For the study, the team used cell cultures from the human respiratory tract. To mimic the airways of asthmatics, they treated some samples with a small protein known to be more common in asthma called interleukin-13 (IL-13). Its presence causes asthmatics to increase mucus production beyond healthy levels.

They then infected the cell cultures with the SARS-CoV-2 virus. In IL-13-treated cells, the coronavirus had difficulty entering the cell to replicate and spread copies of itself. At the same time, there were much more infections in untreated cells.

“We knew there must be a biomechanistic reason why people with allergic asthma seem to be more protected from severe disease,” says UNC biochemist Camille Héré.

“Our research team found a number of significant cellular changes, especially under the influence of IL-13, leading us to conclude that IL-13 plays a unique role in protecting against SARS-CoV-2 infection in certain patient populations.”

By observing the interaction of respiratory cells and the virus under an electron microscope, Ehre and her colleagues noticed that IL-13 treatment significantly reduced the number of infected cells while simultaneously increasing the amount of mucus produced by those cells.

However, even when the mucus was removed, the cells still showed some degree of protection against the invading coronavirus.

RNA sequencing has confirmed that the presence of IL-13 in cell culture increases the level of genes associated with antiviral properties and reduces the expression of cellular receptors to which coronaviruses are known to attach, such as ACE2.

In untreated respiratory cells, these receptors allow the coronavirus to invade the body with relative ease. If the cell is indeed infected, the researchers noticed that it was more likely to break away from the surface of the airways, allowing it to travel deeper into the lungs, thereby spreading the infection.

“In conclusion, the vigorous viral and cell proliferation induced by SARS-CoV-2 infection was attenuated by IL-13, which affected virus entry, replication, and spread,” the authors conclude.

Unfortunately, IL-13 cannot be used as a treatment on its own. It is part of the immune response, which means it can cause inflammation in a patient’s airways.

But understanding the subtleties of what is happening in the lungs is still extremely important. By comparing cells that mimic the airways of asthmatics with healthy cells in the airways, scientists have uncovered some of the underlying mechanisms behind severe cases of COVID-19.

In the future, therapeutic drugs could help target specific areas that appear to be more involved in severe symptoms.

“We believe this study shows once again how important it is to treat SARS-CoV-2 infection as early as possible,” says Ehre.

“And it shows how important specific mechanisms involving ACE2 and IL-13 are as we struggle to protect patients from developing severe infections.”


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