The study also said that drugs aimed at endothelial activation should be used to control inflammation and coagulopathy associated with COVID-19.
Structure and cross section of human coronavirus. It shows the shape of the coronavirus, as well as the cross section. The image shows the major elements, including Spike S protein, HE protein, viral envelope and helical RNA. Image credit: Wikipedia
COVID-19 it is primarily a respiratory disease that spreads through drops. COVID-19 causing coronavirus , SARS-CoV-2, enters the body through the mouth or nose and uses the ACE2 receptors present on the surface of host cells to infect these cells. Because the virus mainly infects the lungs and airways, patients can suffer from lung damage, inflammation of the endothelium (the inner surface of blood vessels) and organ dysfunction.
Patients also have increased blood clotting and the formation of small blood clots in the body. However, until now it was not known whether SARS-CoV-2 actually deregulates vascular function.
Now, a group of researchers at Stony Brook University, USA, states that endothelial cells do not have ACE2 receptors and therefore SARS-CoV-2 does not infect these cells directly. However, because endothelial lesions are 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-reviewed journal mbio.
Indirect infection of endothelial cells
For the study, the researchers examined SARS-CoV-2 infection in endothelial cells (EC) obtained from the lungs, kidneys, heart, brain and umbilical veins. It was found that the virus did not infect any of the ECs tested.
The research team then introduced the ACE2 gene into the EC and exposed them to SARS-CoV-2. This time a viral titer between 1 and 3 X 107 was found in these cells, indicating that the cells were infected with coronavirus this time. In addition, the study authors suggested that although EC does not express ACE2 receptors, they do express some proteases that SARS-CoV-2 uses to regulate endothelial function. The virus can also infect a small number of endothelial cells, causing inflammation and damage.
Our research has shown that endothelial cells have no ACE2 receptors and that endothelial cells were infected only with SARS-CoV-2 after expressing ACE2 receptors in them. Because the functions of endothelial cells are regulated by SARS-CoV-2, these findings suggest a new regulatory mechanism that does not require viral infection. Instead, it suggests indirect endothelial activation, which could result from damage to surrounding tissues, which could be the basis for further research to target and restore normal endothelial cell responses, “said Dr. Erich Mackow, lead author of the study. in a news story. launched by Stony Brook University.
Targeting of endothelial cells
Because endothelial cells are not actually infected with SARS-CoV-2, drug therapies against infection would be useless in the treatment of endothelial inflammation in coronavirus patients. Instead, the study’s authors say that drugs that target endothelial activation should be used to control inflammation and coagulopathy associated with COVID-19 .
According to the press release, the Stony Brook research team now intends to study how SARS-CoV-2 or coronavirus -infected lung cells activate EC.
For more information, read our article on Why coronavirus affects the lungs.
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