#Covid spike plus

Surprisingly, they found the heart pericytes were not infected. The team also sought to investigate whether heart cells contribute to producing excess cytokines.Ī research team led by Bristol’s Professor Paolo Madeddu exposed human heart pericytes, which are cells that wrap small blood vessels in the heart, to SARS-CoV-2 Alpha and Delta variants, along with the original Wuhan virus. This response, also known as ‘the cytokine storm’, comes from our immune cells, whereby cytotoxic cells attack and kill the infected cells by releasing proteins, called cytokines. Until now, it remained unclear whether heart cells are infected by the virus or damaged because of an excess cytotoxic defence response. In this new study, published in the journal Clinical Science, a multidisciplinary research team from the University’s Bristol Heart Institute sought to investigate how SARS-CoV-2 interacts with heart cells causing the myocardial damage seen in COVID-19 patients. The University of Bristol-led research, published in Clinical Science, indicates blocking antibodies could represent a new treatment to alleviate cardiovascular complications.

Makowski hopes his hypothesis will spur other researchers to investigate further.įor media inquiries, please contact Shannon Nargi at or 61.A new study has shown how SARS-CoV-2 may contribute to severe microvascular damage seen in severely-ill COVID-19 patients by transforming human heart vascular cells into inflammatory cells, without infecting them. Uncovering the cause of that coagulation is the next step. “Now if you end up in the ICU, you almost always get an anticoagulant, and that saves a lot of lives.” Recognizing that coagulation is a major problem has greatly improved the survival rate of people who are severely sick with COVID-19, Makowski says. 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.

#Covid spike plus

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.