The coronavirus SARS-CoV-2 can more easily cling to human airway cells type A blood compared to those with type B or O blood, a new study indicates. The findings suggest a possible explanation for why studies throughout the pandemic have found that those with type A blood are more likely to catch COVID-19 and develop severe symptoms than other blood groups.
Laboratory experiments revealed that part of the coronavirus called the “receptor binding domain” (RBD), which binds directly to cells to initiate infection, also reaches out to unique molecules associated with type A blood. These molecules, known as antigens, appear in cells that line the airways, including the longeaccording to the study, which was published in the journal on March 3 Blood transfusion.
In theory, binding to these structures could help the coronavirus to enter and infect the airway cells more easily, but we do not know for sure yet, the authors told WordsSideKick.
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‘Does it affect the ability of the virus to get into cells? Does it just affect the ability to adhere to the cells? ‘, The study author, dr. Sean Stowell, a medical-scientist from a transfusion medicine, said with appointments at Brigham and Women’s Hospital in Massachusetts and Emory University in Georgia. ‘ It’s open. We’re working on it now, but the jury is still unavailable. ‘
In other words, the data provide the first physical link between the coronavirus and type A blood, but more research is needed to confirm that this difference affects the chance of actual infection.
Why would blood type matter?
Since the early days of the pandemic, several studies of coronavirus patients have discovered trends in which blood groups are most prevalent, Live Science reported earlier.
“In many studies, there is a link between blood groups and propensity for SARS-CoV-2 infections,” especially showing that people with type O blood have a lower risk of catching COVID-19, in comparison with non-O blood groups, says dr. Torben Barington, a 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 found.
“Several hypotheses have been proposed for these associations, but we have yet to learn what the mechanisms are,” Barington said in an email to WordsSideKick. This new study suggests a possible explanation for why SARS-CoV-2 can infect blood group A more easily than type O – although that does not explain why type B is also linked to more infections than type O, he noted.
Stowell said he and his colleagues were curious about the link between blood type and COVID-19, but that they actually got inspiration for their new study while developing a diagnostic test for the disease.
While doing the test, “we started looking at different parts of the virus and realized that the receptor binding domain … it looks a lot like an ancient group of proteins called galectins,” Stowell said.
Galectins can be found in all multicellular animals and bind to carbohydrates, or sugar structures, known as glucans; In humans, galectins can be found throughout the body and participate in many processes, from muscle development to metabolism to immune cell behavior, Stowell said.
In the past, “we have noticed that galectins really like to bind to antigens in the blood group”, proteins and molecules that are specific to different blood groups, and off the surface of the cells. Blood group antigens come in two flavors – A and B – and the presence or absence of these antigens determines the blood group of a person – A, B, AB, who has both, or O, who does not have one, according to the American Red Cross. The antigens are found not only on blood cells in the body, but also on other tissues, including the lining of the lungs.
Given the molecular similarity between the coronavirus RBD and galectins, ‘we thought’ Well, maybe the virus binds directly to antigens in the blood group, ‘Stowell said. If this is the case, blood group antigens could somehow affect the likelihood of infection, he said. For example, some viruses get on cells by first seizing glycans on their surfaces, according to a 2016 report in the journal Current opinion on structural biology; the viruses then release these glucans to slip through nearby entrances into the cell, causing infection.
Something similar could possibly happen with blood group antigens and SARS-CoV-2, the authors thought. With this hypothesis in hand, the team went to the laboratory to perform experiments.
In the laboratory
The team analyzed how the RBD interacted with red blood cells isolated from individuals of group A, B, and O; they also performed experiments with synthetic blood group antigens, based on antigens found on both respiratory and red blood cells from the three blood groups. This enabled the team to compare whether and how the RBD binds to blood group antigens in the blood cells and in the airways.
“The odor of blood group antigens that is expressed on the surface of red blood cells is slightly different from the taste that our lungs carry,” Stowell noted. Because of their different molecular structures, the antigens specifically bind to respiratory cells a little differently than to blood cells, he said.
What is interesting is that this subtle difference seems to matter to the RBD of the coronavirus, he said. Based on the experiments, the RBD does not readily bind to any of the red blood cell antigens and shows no preference between the blood groups. In contrast, the RBD was ‘highly preferred’ for the type A antigens found in respiratory cells.
“It was clear; there was this preference. We did not expect it,” Stowell said. Now, “whether that actually means the virus is more likely to infect blood group A, I would say, we do not know.”
As these data were obtained from laboratory experiments, the result may not perfectly reflect what is happening in the country. human body, said Fumiichiro Yamamoto, an immuno-hemologist 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 the scenarios tested in laboratory experiments, Yamamoto told WordsSideKick via email. In addition, other substances in the body compete to bind to the same antigens of the blood type, so it is unclear how many coronavirus particles would eventually sound, he added.
What’s more, the 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 may also bind to these free-floating antigens, which can reduce the number of viral particles that reach the respiratory cells, he said.
And in addition to unique antigens, different blood groups also contain specific blood groups antibodies, molecules that help Immune system to eliminate foreign invaders, Barington said. These antibodies are particularly prevalent in individuals with blood type O and it has been suggested that virus be neutralized on our mucosal surfaces, he said. It could be that both blood group antigens and antibodies affect the likelihood of COVID-19 infection, and that their individual contributions need to be sorted out, he said.
As for the new study, “it’s an important first step,” Stowell said. ‘The critical thing to do [now] is to determine whether the actual virus, in terms of its ability to infect cells, is affected by antigens of the blood group or not. ‘
Originally published on Live Science.