During the COVID-19 pandemic, researchers explored whether a person’s inherited blood type, specifically the ABO group, might influence their risk of contracting the SARS-CoV-2 virus or the severity of the resulting illness. Understanding the role of these common genetic markers offers insights into the complex biological interactions between the virus and the human host. Studies have sought to clarify if blood type represents a slight predisposition or protection against the infection.
Understanding the ABO Blood Group System
The ABO system classifies blood into four main groups—A, B, AB, and O—based on carbohydrate molecules, known as antigens, found on the surface of red blood cells. Type A blood possesses the A antigen, Type B possesses the B antigen, and Type AB has both A and B antigens. Type O lacks both the A and B antigens entirely.
A person’s plasma naturally contains antibodies against the antigens their own red cells do not possess. For instance, individuals with Type O blood have both anti-A and anti-B antibodies in their plasma, while Type A individuals have anti-B antibodies. These ABO antigens are also expressed on the surface of endothelial cells lining blood vessels and on various epithelial cells throughout the body, including in the respiratory tract. This widespread presence makes the ABO system potentially relevant to a systemic infection like COVID-19.
Observed Correlation with Infection Susceptibility
Large-scale epidemiological studies have consistently found a statistical correlation between ABO blood type and the likelihood of becoming infected with SARS-CoV-2. Data suggests that individuals with Type O blood have a slightly lower risk of contracting the virus compared to those with non-O blood types. Conversely, Type A blood has been associated with a slightly increased susceptibility to initial SARS-CoV-2 infection.
These findings point to a modest, recurring pattern across diverse global populations, indicating a statistical predisposition, not absolute protection or guaranteed infection. The difference in risk is minor, suggesting that blood type is only one of many factors influencing infection risk, alongside exposure, age, and underlying health conditions. Type B and Type AB individuals generally show intermediate risks, often falling between the patterns observed for Type A and Type O.
Blood Type and Disease Severity
Research has explored whether blood type influences how severely COVID-19 progresses once a person is infected. Studies suggest that the protective effect seen in Type O blood may extend to clinical outcomes, with Type O patients exhibiting a lower risk of severe illness, hospitalization, or death. This group has been associated with a decreased risk of developing COVID-19 pneumonia and requiring mechanical ventilation.
In contrast, Type A blood has frequently been linked to a higher risk of developing severe COVID-19 symptoms that necessitate intensive care unit (ICU) admission. Type A patients have also been associated with longer lengths of hospitalization compared to other blood groups. This pattern suggests that the genetic factor determining the A antigen may affect both initial susceptibility and the body’s inflammatory or coagulation response to the infection. The recurring signal suggests that Type A blood may represent a minor risk factor for a worse clinical trajectory, while Type O may offer a small degree of protection against serious complications.
Hypothesized Biological Mechanisms
One leading hypothesis for the susceptibility difference involves the naturally occurring antibodies found in the blood. Type O individuals possess anti-A antibodies, which could potentially neutralize the virus or block its attachment if the SARS-CoV-2 spike protein mimics the A antigen. This mechanism would offer a form of pre-existing immunity, explaining the lower infection rates for Type O individuals.
A second mechanism relates to the established link between ABO blood type and the body’s clotting system. Individuals with Type O blood typically have plasma levels of von Willebrand factor (vWF) and Factor VIII that are approximately 20 to 30 percent lower than in non-O blood types. These two factors play a major role in blood clotting and are frequently elevated in severe COVID-19 cases, contributing to dangerous hypercoagulability and thrombosis.
The A antigen is present on the vWF molecule, and its presence is thought to interfere with the activity of ADAMTS13, an enzyme that breaks down vWF. Because Type O blood lacks the A antigen, the vWF in these individuals is cleaved more efficiently. This results in lower circulating levels, potentially reducing the risk of severe blood clots associated with COVID-19. This difference in coagulation protein levels may explain why Type O blood correlates with less severe disease outcomes.