One of the biggest issues that many individuals fighting severe COVID-19 face is an overactive immune response. In effort to protect itself, the body creates dangerous levels of inflammation. Then, healthy cells can begin to be attacked, only damaging the body further.
A research team at Johns Hopkins has just made a new discovery that may help to combat this impact of COVID. Senior author on this study was Robert Brodsky. The study was published in Blood.
The Study
This research team evaluated the moment when the virus binds to the healthy cells. The spikes of SARS-CoV-2 attach to heparin, which is a sugar molecule. Heparan is present within the blood vessels, the muscles, and the lungs. During this process, the virus stops factor H from attaching to cells. When factor H isn’t bound to these cells, they are vulnerable to attacks from the immune system.
Factor D is also involved in this process, a little further down the line. Because of this, the team thought that if they could inhibit factor D, they could stop the body from having such an extreme immune response. Testing this, they found that this was a successful methodology and the virus was not able to activate the other complement pathway.
Currently, Alexion is developing a Factor D inhibitor. A Phase 3 trial examining Ultomiris, a different complement-related drug, was launched for patients with severe disease back in April. This drug works to inhibit terminal complements. The therapy has already been approved by the FDA to treat some rare blood conditions.
An Additional Study
A research team at Imperial College in London has also completed a study, recently published in Frontiers in Immunology.
They found that Foxp3 plays an important part in mediating the immune response that COVID-19 incites. This protein was uncovered through a study of six tissue samples from severely sick COVID-19 patients. Additionally, three samples were taken from patients who were moderately ill, and three were taken from healthy individuals. All of the samples in this study were taken from patients living in China.
It was found that the most severely sick patients had hyperactive T cells within their lungs. This indicates that a dangerous inflammatory immune response is occurring. Foxp3 typically helps to moderate this response so that it doesn’t go too far. Unfortunately, in the sickest COVID-19 patients, none of this protein was found.
Future investigations are being planned by this team to better understand how this protein is involved in the virus, with the hope that we can eventually determine a way to stop the overactive immune system.
You can read more about these studies here.
