A modeling study by Dr. Peter Ellis from the University of Kent indicates that ABO incompatibility between infected patients and susceptible individuals may actually decrease the transmissibility of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by 60% or more. His detailed investigation of such “ABO-interference” can be found on the medRxiv* preprint server.
Certain aspects of an ongoing pandemic of coronavirus disease (COVID-19), caused by SARS-CoV-2, is still baffling population-level epidemiologists. Meanwhile, researchers across the globe are racing to find an effective treatment or vaccine.
Previous work on human immunodeficiency virus (HIV), measles, and enveloped viruses, in general, showed that the viral spread might be reliant on the ABO blood type compatibility between an infected person and the susceptible individuals they encounter.
COVID-19 and blood type
Accordingly, several preprints and studies published recently have hinted that the prevalence of COVID-19 can vary significantly by blood type, with type A being relatively susceptible to the disease, and type O being less susceptible.
News Medical recently reported on extensive genetic analysis that also showed how individuals with blood type O seemed to be protected against the severe forms of the disease. In contrast, blood type A can predispose them to complications related to the viral infection. However, the pertinent question is whether we can incorporate these findings into prevailing epidemiological models.
In this paper, Dr. Peter Ellis, a Lecturer in Molecular Genetics and Reproduction at the University of Kent School of Biosciences in Canterbury, UK, develops a theoretical model in which ABO transfusion incompatibility basically reduces the chance of transmitting SARS-CoV-2 from a patient to an incompatible recipient.
Super-spreaders and super-recipients
“The model presented here shows that if ABO-interference is the cause of the widely observed bias in SARS-CoV-2 infection rates among different blood types, then ABO incompatibility reduces SARS-CoV-2 transmission by at least 60% and potentially more”, explains Dr. Ellis.
However, it is vital to take into account that no blood type necessarily confers high-risk or low-risk, as the nature of any protection is entirely context-dependent.
More specifically, the existence of a diverse blood type mix within any given community (i.e., in the pool of individuals that freely mix and may consequently transmit the virus to each other) provides significant protection. The opposite is valid for communities with limited blood type diversity.
Generally speaking, such heterogeneity in transmissibility indicates that the risk to non-O (in particular type AB) individuals in most countries will be higher than the risk to type O individuals, whereas individuals with type O are more infectious than non-O ones. This pinpoints both “super-spreaders” and “super-recipients.”
“This study also showed via modeling that ABO-interference could reduce the progress of an epidemic dependent on the magnitude of the block to the transmission and the local population structure,” says Dr. Ellis.
Testing the model
The key experiment in testing this model will be to directly appraise whether A or B antigens can be found on the virus envelope and whether A- or B-specific antisera can neutralize the virus from patients with appropriate blood types.
But other testable predictions may be addressed with the use of existing epidemiological data. For example, in studies of super-spreading events, all index cases should be disproportionately blood type O.
Moreover, in countries that have a high frequency of blood type B (such as India), those individuals should be at higher risk in comparison to type A. Also, direct contact-tracing data should generally follow the blood transfusion rules.
Optimizing the vaccine strategy
In any case, any vaccination strategy that will be introduced in the future should not disrupt the intrinsic protection afforded by ABO-interference. It seems logical that a well-devised strategy of reducing infection rates might prioritize the vaccination of type O super spreaders before type A.
Nonetheless, once all type O individuals are immunized, the protective effect of ABO-interference is eliminated as the remaining ones are now exclusively type A. And any infected type A individual is able to transmit the infection to any prevailing susceptible individual freely.
This is becoming increasingly important, as promising vaccine candidates already entered phase III clinical trials. Therefore, similar modeling approaches are needed to avoid overly simplistic vaccine strategies that may result in skewed herd immunity estimates.