The SARS-CoV-2 coronavirus can attach itself more easily to cells in the airways of people with the disease type A blood compared to those with type B or O blood, a new study suggests. The results suggest a possible explanation for why, throughout the pandemic, studies have shown that people with type A blood are more likely to catch COVID-19 and develop severe symptoms than those with type A blood. other blood groups.
Laboratory experiments have revealed that part of the coronavirus called a ‘receptor binding domain’ (RBD), which binds directly to cells to trigger infection, also attaches itself to unique molecules associated with type A blood. These molecules, called antigens, appear on cells that line the airways, including the lungs, according to the study, published on March 3 in the journal Advances in blood.
In theory, binding to these structures may help the coronavirus to enter and infect airway cells more easily – however, we don’t yet know for sure, the study’s authors told Live Science.
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“Does this really influence the ability of the virus enter the cells? Does it just influence its ability to adhere to cells? Said study author Dr. Sean Stowell, a physician-scientist in transfusion medicine with appointments at Brigham and Women’s Hospital in Massachusetts and Emory University in Georgia. We’re working on this right now, but the jury is still out. “
In other words, the data provides the first physical link between the coronavirus and type A blood, but more research is needed to confirm that this difference affects the chances of actual infection.
Why is blood type important?
Since the early days of the pandemic, several studies of coronavirus patients have found patterns in the blood groups that appear to be most commonly infected, Previously reported Live Science.
“Many studies have found associations between blood groups and the propensity for SARS-CoV-2 infections”, in particular, showing that people with type O blood have a lower risk of catching COVID-19, compared to non-O blood groupssaid Dr Torben Barington, clinical immunologist at Odense University Hospital and the University of Southern Denmark, who was not involved in the study. People with type A blood may also be more likely to develop severe symptoms and respiratory failure when they contract the virus. some studies have found.
“Several hypotheses have been proposed for these associations, but we still have to know what the mechanisms really are,” Barington told Live Science in an email. This new study suggests a possible explanation for why SARS-CoV-2 can infect individuals with blood group A more easily than type O – although this does not explain why type B is also linked to more d. infections than type O, he noted.
Stowell said he and his colleagues were curious about the blood group’s connection to COVID-19, but actually inspired their new study while developing a diagnostic test for the disease.
When creating the test, “we started looking at different parts of the virus and realized that the receptor binding domain… it looks a lot like an old group of proteins called galectins,” Stowell said.
Galectins can be found in all multicellular animals and bind to carbohydrates, or sugar structures, known as glycans; in humans, galectins can be found throughout the body and are involved in many processes, from muscle development and metabolism to the behavior of immune cells, Stowell said.
In the past, “we have observed that galectins love to bind to blood group antigens,” proteins and molecules specific to different blood groups that stick to the surface of cells. Blood group antigens come in two flavors – A and B – and the presence or absence of these antigens determines a person’s blood group – A, B, AB, which has both, or O, which does not. neither one nor the other, according to the American Red Cross. Antigens are found not only on the body’s blood cells, but also on other tissues, including the lining of the lungs.
Considering the molecular similarity between the RBD coronavirus and galectins, “we thought, ‘Well, maybe the virus binds directly to blood group antigens,” “Stowell said. If so, blood group antigens could somehow influence the likelihood of infection taking hold, he said. For example, some viruses accumulate on cells by first grabbing glycans on their surface, according to a 2016 report in the journal. Current opinion in structural biology; the viruses then release these glycans to slip through the entrances close to the cell, triggering an infection.
Something similar could potentially happen with blood group antigens and SARS-CoV-2, the authors thought. With that hypothesis in hand, the team headed to the lab to conduct experiments.
In the lab
The team analyzed how RBD interacted with red blood cells isolated from individuals of blood groups A, B and O; they also conducted experiments with synthetic blood group antigens, based on antigens found on both red blood cells and respiratory cells of all three blood groups. This allowed the team to compare whether and how RBD binds to blood group antigens on blood cells and in the airways.
“The flavor of blood group antigens that are expressed on the surface of red blood cells is slightly different from the flavor that lines our lungs,” noted Stowell. Specifically, due to their different molecular structures, antigens bind a little differently to respiratory cells and blood cells, he said.
What’s interesting is that this subtle difference appears to matter for the coronavirus RBD, he said. Based on the experiments, RBD does not readily bind to any of the red blood cell antigens and does not show any preference between blood groups in this regard. In contrast, RBD “showed a high preference” for type A antigens found on respiratory cells.
“It was clear; there was this preference. We weren’t expecting that,” Stowell said. Now, “if that really means the virus is more likely to infect blood type A, I would say, we don’t know.”
Since these data were taken from laboratory experiments, the result may not fully reflect what is happening in the human bodysaid Fumiichiro Yamamoto, an immunohematologist at the Josep Carreras Leukemia Research Institute in Barcelona, who was not involved in the study.
“The binding may or may not reflect the actual situation on the cell surface,” especially since the density of antigens on the cell surface may differ from scenarios tested in lab experiments, Yamamoto told Live Science in an email. Additionally, in the body, other substances compete to bind to the same blood group antigens, so it’s unclear how many particles of the coronavirus would end up clinging, he added.
What’s more, type A antigens found on the surface of airway cells can also be secreted elsewhere in the body, such as in saliva, he said. This means that the virus could potentially bind to these floating antigens, thereby reducing the number of viral particles that reach respiratory cells, he said.
And in addition to unique antigens, different blood groups also carry a specific blood group antibody, molecules that help immune system eliminate foreign invaders, Barington said. These antibodies are particularly “prevalent in individuals with blood group O and have been proposed to neutralize the virus on our mucous surfaces,” he said. Blood group antigens and antibodies may influence the likelihood of COVID-19 infection, and their individual contributions will need to be sorted out, he said.
As for the new study, “this is an important first step,” said Stowell. “The critical thing to do [now] is to determine whether the virus itself, in terms of its ability to infect cells, is influenced by blood group antigens or not. “
Originally posted on Live Science.