A new study conducted by a researcher from Canada has uncovered how the novel coronavirus kills the host, offering possible ways to contain the virus pandemic.

The research by Douglas Fraser from the Lawson Health Research Institute in Canada was published in the journal Critical Care Explorations. It revealed that the major complication in patients adversely affected by the virus is clotting in the blood vessels of the lungs. This further leads to low oxygen levels in the body.

Study author Fraser said in a statement: “While the findings need to be validated with larger groups of patients, they could have important implications for treating and studying this disease.”

“The reason for this clotting has been unclear. Most suspect the clotting mechanisms in our blood are put into overdrive and so many clinicians have been treating with anticoagulant therapies like the drug heparin. But we’ve uncovered an entirely different mechanism,” Fraser added.

For the initial part of the research, Fraser and the team measured 1,161 plasma proteins from the blood of 30 participants: 10 Covid-19 patients and 10 patients with other infections admitted to ICU, as well as 10 healthy control participants.

Blood was collected from them after their admission to ICU. It was then processed in a lab and analysed using statistical methods and artificial intelligence.

The team inferred that speculating the severity of the virus in patients’ disease can help in a number of ways. It could allow for medical teams to have important conversations with family members, setting goals of care based on the patient’s health and personal wishes.

For the second part of the research, the team examined the blood samples from the 30 participants and found evidence to suggest that the inner linings of small blood vessels are becoming damaged and inflamed, making them a welcoming environment for platelets (small blood cells) to stick. They discovered that Covid-19 patients had elevated levels of three molecules (hyaluronic acid, syndecan-1, and P-selectin.)

The first two molecules are products broken down from small hair-like structures (the glycocalyx) which line the inside of the blood vessels.

Their presence suggested the glycocalyx was damaged with its breakdown products sent into the bloodstream.

The presence of P-selectin is also significant as this molecule helps to make both platelets and the inner lining of blood vessels adhere to one another.

“The glycocalyx keeps platelets from touching the inside wall of the blood vessel and helps facilitate the production of nitric oxide, which has an important role in preventing platelets from sticking,” explained Fraser.

“We suspect the body’s immune response is producing enzymes that shear off these little hair-like structures, inflaming blood vessels and making them a welcoming environment for platelets to form clots,” Fraser said.

The team recommended two therapies to treat the blood clot in patients: platelet inhibitors to stop platelets from sticking and molecules to protect and restore the inner lining of blood vessels.