The SARS-CoV-2 coronavirus can more easily attach to airway cells in people with blood type A compared to those with type B or O blood, a new study suggests. The findings suggest a possible explanation for why, during the pandemic, studies found that people with type A blood are more likely to get COVID-19 and develop severe symptoms than other blood types.
Laboratory experiments revealed that part of the coronavirus called the “receptor-binding domain” (RBD), which binds directly to cells to initiate infection, it also clings to unique molecules associated with type A blood. These molecules, known as antigens, appear in the cells lining the tract respiratory, including lungs, according to the study, published on March 3 in the journal Blood advances.
In theory, attachment to these structures can help the coronavirus enter and infect airway cells more easily – however, we’re not sure yet, the study’s authors told Live Science.
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“It really influences the ability of the virus enter the cells? Does this only influence your ability to adhere to cells? “Said the study’s author, Dr. Sean Stowell, a medical scientist in transfusion medicine with consultations at Brigham and Women’s Hospital in Massachusetts and at Emory University in Georgia.” This is open. We are working on it now, but the jury has not yet decided. “
In other words, the data provide the first physical link between coronavirus and type A blood, but more research is needed to confirm that this difference affects the chances of real infection.
Why does blood type matter?
Since the early days of the pandemic, several studies of patients with coronavirus have found trends in which blood types appear to be infected most often, Live Science previously reported.
“Many studies have found associations between blood groups and a propensity for SARS-CoV-2 infections”, in particular, showing that people with type O blood have an lower risk of catching COVID-19, compared to blood types not Osaid 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 still need to learn what the real mechanisms are,” Barington told Live Science by email. This new study suggests a possible explanation for why SARS-CoV-2 can infect type A individuals more easily than type O – although it 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 were actually inspired by 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 … is very similar to an old group of proteins called galectins,” said Stowell.
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 participate in many processes, from muscle development to the metabolism and behavior of immune cells, said Stowell.
In the past, “we observed that galectins really love to bind to blood group antigens”, proteins and molecules that are specific to different blood groups and attach 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 has neither, according to the American Red Cross. Antigens are found not only in the body’s blood cells, but also in other tissues, including the lining of the lungs.
Given the molecular similarity between the RBD coronavirus and galectins, “we thought, ‘Well, maybe the virus binds directly to blood group antigens,'” said Stowell. If that is the case, blood group antigens may somehow influence the likelihood that the infection will spread, he said. For example, some viruses accumulate in cells, first grabbing glycans from their surfaces, according to a 2016 report in the newspaper Current Opinion in Structural Biology; the viruses then detach themselves from these glycans to infiltrate the entrances near the cell, triggering the infection.
Something similar could be happening to blood group antigens and SARS-CoV-2, the authors thought. With this hypothesis in hand, the team went to the laboratory to carry out experiments.
In the lab
The team analyzed how RBD interacted with red blood cells isolated from individuals in blood groups A, B and O; they also carried out experiments with synthetic blood group antigens, based on antigens found in the respiratory cells and red blood cells of the three blood groups. This allowed the team to compare whether and how RBD binds to blood group antigens in blood cells and the airways.
“The taste of blood group antigens that are expressed on the surface of red blood cells is slightly different from the taste that lines our lungs,” noted Stowell. Specifically, due to their different molecular structures, antigens bind slightly differently to respiratory cells than to blood cells, he said.
What’s interesting is that this subtle difference seems to matter for coronavirus RBD, 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 blood types in this regard. In contrast, RBD “exhibited high preference” for type A antigens found in respiratory cells.
“It was clear; there was that preference. We didn’t expect that,” said Stowell. Now, “if it really means that the virus is more likely to infect blood group A, I would say, we don’t know.”
Given that these data were extracted from laboratory experiments, the result may not reflect perfectly what happens in the Human Body, said Fumiichiro Yamamoto, an immunohematologist at the Leukemia Research Institute Josep Carreras in Barcelona, who was not involved in the study.
“The connection 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 the laboratory experiments, Yamamoto told Live Science by email. In addition, in the body, other substances compete to bind to the same blood group antigens, so it is unclear how many particles of coronavirus would eventually get trapped, he added.
In addition, type A antigens found on the surface of airway cells can also be secreted in other parts of the body, such as saliva, he said. This means that the virus can potentially bind to these floating antigens, decreasing the number of viral particles that reach respiratory cells, he said.
And, in addition to unique antigens, different blood types also carry specific blood groups antibodies, molecules that help the immune system eliminate foreign invaders, said Barington. These antibodies are particularly “prevalent in group O individuals and have been proposed to neutralize the virus on our mucous surfaces,” he said. It may be that both blood group antigens and antibodies influence the likelihood of COVID-19 infection, and their individual contributions need to be assessed, he said.
Regarding the new study, “it is an important first step,” said Stowell. “The critical thing to do [now] is to determine whether the real virus, in terms of its ability to infect cells, is influenced by blood group antigens or not. “
Originally published on Live Science.