But either way, a faulty connection between RGD and integrin could be the culprit. Makowski hypothesizes that dysregulated blood vessel growth-which can disrupt lung tissue-is triggered by an increase of RGD during infection.Īs for COVID-19-related kidney failure, “it’s hard to know whether it’s caused by direct damage to the tissue by viral invasion or indirect damage through coagulation and blocked arteries,” Makowski says. “But our theory is that because has an RGD, it may also be more likely to bind to other cells in the body that people aren’t thinking about,” Olson-Sidford says. ACE2 is found in many cell types including in the lungs, heart, blood vessels, kidneys, liver, and gastrointestinal tract. Right now, researchers know that the virus’s spike protein binds to cell receptors called ACE2. Our theory is that RGD is making it easier for the virus to bind to things that could cause these blood complications,” says William Olson-Sidford, a third-year bioengineering student and co-author of the paper who worked on this project as a co-op last fall. “Other proteins that have RGD are known to cause complications. Researchers don’t know yet whether RGD is the culprit for COVID-19’s blood-related complications, but they do know that RGD can contribute to the formation of blood clots and the growth of new blood vessels when it interacts with cell receptors called integrins. Photos by Matthew Modoono/Northeastern University William Olson-Sidford, who studies bioengineering, works on SARS-CoV-2 research in Lee Makowski's lab inside the the Interdisciplinary Science and Engineering Complex. This structure is known for connecting cells to each other in the body. At the tip of the spike protein rests a string of three amino acids called RGD. The spike protein is an arm-like apparatus that the virus uses to attach to and enter healthy cells. Makowski, who recently published his hypothesis in the journal Viruses, believes the spike protein found on the surface of the virus might mimic proteins that regulate blood vessels and control the formation of blood clots, which could explain many of the non-respiratory complications of COVID-19. “One of the most perplexing and devastating effects of this disease is the scenario where three or four weeks after being hospitalized with pneumonia, people under the age of 50 are back home, they feel fine, and then all of a sudden they have a stroke and die,” says Makowski, professor and chair of the bioengineering department at Northeastern. The postmortem evidence plus his own experience with something called “COVID toes”-an odd side effect of the disease that causes heightened blood vessel formation in the toes, turning them bright red-led Makowski to speculate that something about the virus might be causing abnormal blood-related complications. Photo by Matthew Modoono/Northeastern University Lee Makowski, chair of the bioengineering department at Northeastern.
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