ISLAMABAD, June 30 (APP): A new study explores the interactions between airway cells and immune cells at the molecular level to identify why some people are at risk of severe COVID-19 while others are not.
There is plenty of evidence that SARS-CoV-2, the new coronavirus, affects individuals differently. About 80% of those who have SARS-CoV-2 experience a clinically mild version of COVID-19, meaning that they get better without needing to go to the hospital.
Risk factors for severe disease include being male, being older, and having underlying health conditions, among other factors. What drives these risk factors is not entirely clear.
Some experts have suggested that an excessive immune reaction in response to the virus is at the heart of the damage to the lungs and other parts of the body that people with severe COVID-19 experience.
Writing in Nature Biotechnology, scientists from the Center for Digital Health at the Berlin Institute of Health (BIH) and the Charité – Universitätsmedizin Berlin in Germany aimed to tease out the molecular actions that underpin such excessive immune reactions.
Prof. Roland Eils, chair and founding director of the Center for Digital Health, is one of the five senior study authors.
To pinpoint how different cells interact and communicate with each other, the multidisciplinary research team performed a single cell RNA sequencing analysis of upper and lower respiratory tract samples from 19 people in the hospital with COVID-19 and five volunteers without the new coronavirus.
In total, the scientists analyzed 160,528 individual cells.
Of the 19 people with COVID-19, eight had moderate disease, the authors write, while they classed 11 as critical. Two people died from the disease.
In the participants with COVID-19, the team saw a three-fold increase in gene expression of the angiotensin converting enzyme 2 (ACE2) gene, which encodes the receptor that the new coronavirus uses to attach to cells during infection.
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