The COVID-19 pandemic prompted extensive scientific inquiry into factors influencing susceptibility and disease progression. Among these, the potential link between an individual’s blood type and their risk for SARS-CoV-2 infection or severe illness garnered significant interest. Researchers explored if genetic predispositions, such as ABO blood group, play a role in how people respond to the virus.
Your Blood Type and How Viruses Infect Cells
Human blood types (A, B, AB, and O) are distinguished by specific carbohydrate molecules, known as antigens, found on the surface of red blood cells. These distinctions arise from inherited genes that determine which antigens are expressed. Type A blood possesses A antigens, Type B displays B antigens, and Type AB features both. Individuals with Type O blood do not express A or B antigens. The ABO system is complemented by the Rh factor, further classifying blood groups.
The SARS-CoV-2 virus begins its infection process by interacting with human cells. Its spike (S) protein binds to the angiotensin-converting enzyme 2 (ACE2) receptor, found on various human cell types. This ACE2 receptor is present in tissues like the lungs, serving as the primary entry point for the virus. After binding, the virus gains access into the host cell, where it replicates and propagates throughout the body, initiating the disease.
What Studies Show About Blood Type and COVID-19
Scientific research has investigated the relationship between ABO blood types and SARS-CoV-2 infection susceptibility. Studies suggest that individuals with Type A blood may have an increased likelihood of contracting the virus. This association has been noted across diverse populations, implying Type A antigens could facilitate viral entry.
In contrast, Type O blood has been consistently linked to a reduced risk of acquiring SARS-CoV-2 infection across global populations. This protective association for Type O individuals is a recurring finding. Some research also indicates that Rh-negative individuals might exhibit a slightly decreased susceptibility to infection.
However, findings are less uniform when examining blood type’s influence on COVID-19 severity, including progression to severe respiratory distress, hospitalization, or mortality. While initial smaller studies reported differences, larger investigations often found no statistically significant association between ABO blood groups and severe symptoms or higher mortality rates.
Potential Biological Links
Scientists are exploring several biological mechanisms to explain the observed associations between blood type and COVID-19 susceptibility. One hypothesis involves natural antibodies. Individuals with Type O blood possess naturally occurring antibodies against A and B antigens. Anti-A antibodies might offer protection against SARS-CoV-2 infection. These antibodies could block the interaction between the viral spike protein and host cell receptors, or aid in viral clearance.
Another proposed mechanism involves the expression of A and B antigens on the surface of various cells. The SARS-CoV-2 spike protein might interact differently with cells expressing these antigens. For example, the virus could bind more readily to cells displaying A antigens, increasing infectivity for Type A individuals. Conversely, the absence of A antigens in Type O individuals might render their cells less susceptible to viral attachment. The role of sialosides in viral binding is also being investigated, as their expression can be influenced by blood group status. These mechanisms require further validation.
Interpreting the Current Findings
When interpreting the current scientific findings regarding blood type and COVID-19, it is important to consider several limitations inherent in many of the studies conducted. A significant number of these investigations were retrospective, meaning they looked back at existing data, which can introduce biases and limit the ability to establish direct cause-and-effect relationships. Such studies often rely on pre-existing records, which may not capture all relevant confounding factors that could influence outcomes. Furthermore, studies varied considerably in their sample sizes, ranging from small cohorts to very large populations, and also differed in demographic characteristics, potentially influencing the generalizability of their results.
The practical implications of the current literature are clear: blood type should not be used as a predictor for an individual’s likelihood of developing severe COVID-19 illness. Public health guidance and medical triage decisions are not supported by the current evidence to incorporate blood type as a factor. Instead, established risk factors such as age, underlying health conditions, and vaccination status remain the primary determinants for assessing risk and guiding preventive measures. Adhering to public health recommendations, regardless of blood type, remains the most effective strategy for mitigating infection and severe disease.