The study’s authors also said endothelial activation medications should be used to control inflammation and coagulopathies associated with COVID-19
The structure and cross-sectional view of human coronavirus. It shows the shape of the coronavirus as well as the cross-sectional view. The picture shows the main elements including the Spike S protein, the HE protein, the virus envelope and the helical RNA. Photo credit: Wikipedia
COVID-19 is primarily a respiratory disease that spreads through droplets. The COVID-19 cause Coronavirus SARS-CoV-2 enters the body through the mouth or nose and infects these cells with the ACE2 receptors present on the surface of the host 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.
Patients also show increased blood clotting and the formation of tiny blood clots in the body. So far, however, it was not known whether the SARS-CoV-2 actually impaired vascular function.
A group of researchers at Stony Brook University in the United States states that endothelial cells do not have ACE2 receptors and therefore SARS-CoV-2 does not directly infect these cells. However, since endothelial damage can be seen in COVID-19 Patients, the authors suggest that the virus indirectly affects endothelial cells. The results of the study will be published in the peer-reviewed journal mbio.
Indirect infection of endothelial cells
For the study, the researchers looked at SARS-CoV-2 infection in endothelial cells (ECs) obtained from the lungs, kidneys, heart, brain, and umbilical cord veins. It was found that the virus did not infect any of the ECs tested.
Next, the research team introduced the gene for ACE2 into ECs and exposed them to SARS-CoV-2. This time a virus titer between 1 and 3 × 10 7 was found in these cells, which indicates that the cells were infected by the Coronavirus this time. Additionally, the study’s authors suggested that while ECs do not express ACE2 receptors, they do express some proteases that SARS-CoV-2 uses to dysregulate endothelial function. The virus can also infect small numbers of endothelial cells, causing inflammation and damage.
“Our research found that endothelial cells lack ACE2 receptors and that endothelial cells were only infected with SARS-CoV-2 after expressing ACE2 receptors. Since the endothelial cell functions are disturbed by SARS-CoV-2, these results suggest a new regulatory mechanism that does not require a virus infection. Instead, this indicates the indirect activation of the endothelium, which may be due to damage to the surrounding tissue and which could form the basis for further research into therapeutic control and restoration of normal endothelial cell responses, ”said Dr. Erich Mackow, lead study author in a news publication by Stony Brook University.
Targeting the endothelial cells
Since 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 Coronavirus Patient. Instead, the study’s authors say that endothelial activation drugs should be used to help control inflammation and coagulopathies related to COVID-19 .
According to the press release, the Stony Brook research team is now planning to investigate how SARS-CoV-2 or Coronavirus -infected lung cells activate ECs.
For more information, see our article on why Coronavirus affects the lungs.
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