The SARS-CoV-2 protein gets into the PALS1 protein and destabilizes it, affecting immune cells. Thus, the inflammatory process is provoked.
Researchers have discovered the cause of the mass destruction of the lungs when infected with a new type of coronavirus infection. They argue that this involves one of the fragments of the SARS-CoV-2 envelope and the PALS1 protein, which is responsible for the adhesion of cells to each other.
“When the virus protein pulls PALS1 out of the cell junction, it could help the virus spread more easily. That would provide a selective advantage for the virus. Any traits that increase the survival, spread, or release of the virus are likely to be retained,” says Liu Qun, a researcher at Brookhaven National Laboratory.
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As a result of infection with SARS-CoV-2, lung tissue is damaged, and its cells die in large quantities. Thus, the development of a severe form of pneumonia is provoked.
Scientists suggest that the most severe consequences of COVID-19 are associated not only with viral particles, but also with disturbances in the functioning of the immune system, as well as lung cells, which they themselves cause.
Experts have developed detailed three-dimensional models of SARS-CoV-2 coat proteins and found out which cellular compounds they can interact with. The experiment showed that one of the fragments of the coronavirus envelope, called Ec18, is able to integrate into the molecules of the PALS1 protein, which plays a major role in connecting lung cells to each other.
“We used two-dimensional averaging and started to see some structural features that are shared among these particles. Our images showed the complex from different orientations but at fairly low resolution,” Liu said.
“Then we use computational tools and computation infrastructure at Brookhaven’s Computational Science Initiative to perform three-dimensional reconstructions. These give us a 3-D model — an experimental map of the structure.”
This was confirmed by further experiments, proving that the protein is incorporated into PALS1, which in this case destabilizes and affects immune cells, creating an inflammatory process.
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In addition, the virus spreads much faster this way.
The results of the work were published in the scientific journal Nature Communications.
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