The study’s authors also said that drugs targeting endothelial activity should be used to control inflammation and coagulopathy associated with COVID-19.
The structure and cross-sectional view of Human Coronavirus. It is shown to visualize the shape of a coronavirus as well as the transverse point of view. An image shows the main elements including the Spike-S protein, HE protein, viral envelope and helical RNA. Image credit: Wikipedia
COVID-19 is primarily a respiratory disease that spreads through droplets. La COVID-19 causing coronavirus , SARS-CoV-2, enters the body through the mouth or nose and uses the ACE2 present on the surface of host cells to infect these cells. Because the virus primarily infects the lungs and airways, patients can suffer from lung damage, inflammation of the endothelium (inner surface of blood vessels) and organ dysfunction.
The patients also show increased blood clotting and the formation of tiny blood clots in the body. However, until now it has not been known whether SARS-CoV-2 actually regulates vascular function.
Now, a group of researchers from Stony Brook University, USA, say that endothelial cells do not have ACE2 receptors and therefore SARS-CoV-2 does not infect these cells directly. However, because endothelial damage is seen in COVID-19 patients, the authors suggest that the virus indirectly affects endothelial cells. The results of the study are published in the peer review mbio.
Indirect infection of endothelial cells
For the study, the researchers examined a SARS-CoV-2 infection in the endothelial cells (EC) obtained from the lungs, kidneys, heart, brain, and umbilical veins. It was found that the virus did not infect some of the tested ECs.
The research team then introduced the gene for ACE2 into ECs and exposed them to SARS-CoV-2. This time a virus titer between 1 and 3 X 107 was found in these cells, indicating that the cells were infected by the coronavirus this time. Additionally, the study authors suggested that although EK does not express ACE2 receptors, they do express some proteases that SARS-CoV-2 uses to deregulate endothelial function. The virus may also infect a small number of endothelial cells, causing inflammation and damage.
“Our research revealed that endothelial cells lack ACE2 receptors and that endothelial cells were only SARS-CoV-2 infected after expression of ACE2 receptors in them. Because the endothelial cell functions are upregulated by SARS-CoV-2, these findings suggest a new “a regulatory mechanism that does not require viral infection. Instead, it suggests the indirect activation of the endothelium, possibly resulting from surrounding tissue damage, which could be the basis for further research to therapeutically target and restore normal endothelial cellular responses,” said Dr. Erich Mackow, main author of the study in news. edition of Stony Brook University.
Aiming at the endothelial cells
Because the endothelial cells are not actually infected with SARS-CoV-2, drug therapies against the infection would be useless in the treatment of endothelial inflammation in coronavirus patients. Instead, the study’s authors say that drugs targeting endothelial activation should be used to control inflammation and coagulopathy associated with COVID-19 .
According to the news, the research team at Stony Brook is now planning to study as a SARS-CoV-2 or coronavirus -infected lung cells activate ECs.
For more information, read our article on Why coronavirus affects the lungs.
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