An unusual phenomenon has been caught in the eyes of scientists as the Omicron mutation has established itself as the dominant species for the novel coronavirus infection (COVID-19). The point is that allergic asthma patients are exceptionally resistant to omicron infection. Photos have nothing to do with the article. /Photo = Getty Images Bank
An unusual phenomenon has been caught in the eyes of scientists as the Omicron mutation has established itself as the dominant species for the novel coronavirus infection (COVID-19). The point is that allergic asthma patients are exceptionally resistant to omicron infection.
Patients with similar chronic diseases, such as chronic obstructive respiratory disease or emphysema, have a very high risk of severe COVID-19.
The research results led by Assistant Professor Camille Ehre of the UNC ‘Marsico Lung Institute’ were published in the Proceedings of the National Academy of Sciences (PNAS) of the United States on the 30th (local time) of last month.
The research team revealed that “Interleukin-13 (IL-13), an inflammatory cytokine (immune protein), played a key role. IL-13 controls host cell ACE2 (angiotensin converting enzyme) expression, It has been shown to inhibit cell infection.
Although the research team confirmed that IL-13 plays a key role in preventing the novel coronavirus infection in asthmatics, they might not use IL-13, which triggers inflammation, as a direct treatment.
Several health factors play a role in the severity of the COVID-19 patient’s condition. Among chronic lung diseases such as COPD, it is interesting to note that allergic asthma patients who are hypersensitive to antigens such as mold, pollen, and animal hair are exceptionally strong once morest COVID-19.
The research team first investigated the mechanism of excretion of foreign substances from airway epithelial cells.
Analysis of the gene sequence of airway epithelial cells infected with the novel coronavirus revealed a singularity in the ACE2 receptor. According to the expression level of ACE2, the type of infected cell and the viral load following infection vary.
The escape of the virus from the ciliary cells of the mucus-covered airway epithelium was also observed through electron microscopy. In addition, it was confirmed that viral infection causes severe pathological changes in cells.
When these changes piled up and reached a climax, the ciliary cells, full of viral particles trapped in the mucus, even came off the airway surface, the research team said.
Dr. Camille Here, who led the study. /Photo = Yonhap News
Professor Ere explained, “The escaped ciliary cells can become a kind of virus reservoir and help spread and spread,” adding, “In addition, the possibility of spreading the infected cells deep into the lung tissue can increase.”
According to the research team, it was confirmed that the infected airway epithelial cells were deficient in the major mucin protein (MUC5AC). However, the viral load continued to increase. This is because the viral infection has progressed so violently that it overwhelms the cells that secrete the mucus protein.
The research team noted that this mucus protein was excessively secreted even in patients with allergic asthma.
We also knew that IL-13 stimulates the secretion of mucin proteins in the lungs when asthma patients are exposed to allergens, so we applied IL-13 to human airway epithelial cells to create a model similar to the airways of asthmatics.
Then, as a result of measuring the viral titer, mRNA level, ciliary cell detachment rate, and total number of infected cells, it was found that all values decreased significantly. Even if the mucus was completely removed from the airway epithelial cells, there was no change in the lowered level.
“This suggests that other factors play a role in IL-13’s protective effect once morest the novel coronavirus,” the research team said.
He continued, “It was IL-13 that upregulates control genes such as glycoprotein synthesis, ion transport, and antiviral processes that are important for immune defense of the airways. It was also involved in suppressing intracellular viral load and intercellular propagation.”
In short, IL-13 had a great effect on the entire process from cell invasion of the virus to proliferation and propagation following penetration, and this action of IL-13 prevented the novel coronavirus from causing serious lung infections. .
“We reaffirmed the need to treat people infected with the novel coronavirus as early as possible to prevent them from progressing to severe disease,” Ere said.
Reporter Lee Bo-bae, Hankyung.com [email protected]