University of Queensland (UQ) researchers have found that the SARS-CoV-2 virus does not infect blood vessels, despite the high risk of blood clots in Covid-19 patients. They found that the cardiovascular complications of Covid-19 are triggered by inflammation caused by infected airway cells.
Dr Emma Gordon and Dr Larisa Labzin from UQ’s Institute for Molecular Bioscience, and Dr Kirsty Short from UQ’s School of Chemistry and Molecular Biosciences, pooled their expertise in vascular biology and virology to determine how the virus causes damage to blood vessels.
“At least 40% of patients that are hospitalised with Covid-19 are at high risk of blood clots, and anti-coagulation therapies are now being routinely used. There have been many studies attempting to prove whether the virus is infecting cells of the inner blood vessel wall or not. By conducting our experiments using real, infectious virus rather than fragments of the virus’s spike protein, we can definitively say it is not,” Dr Gordon said.
The researchers used UQ’s microscopy facilities to track where the virus travelled in the cells and visualise how blood vessels respond to the live virus.
Immunologist Dr Labzin said: “When our immune system works well, it clears the virus from our bodies. But sometimes it goes into overdrive, and we get an overblown inflammatory response causing complications – in the case of Covid-19, this is often blood clots when there shouldn’t be any. Knowing that it is inflammation causing these cardiovascular complications arising from Covid-19, rather than the virus itself, will help us develop the right treatments and a better understanding of how and why these complications arise.”
Heart Foundation interim CEO Professor Garry Jennings said the study helps clarify a key debate about the relationship between the virus and the lining of the blood vessels. He said: “How the cells lining the blood vessels sense the virus and the damage to nearby cells is still not completely understood. There is more research to do, but this study is an important step in our understanding of the virus and which cells and mechanisms we should look at next.”
Dr Emma Gordon and Dr Larisa Labzin
