Want to solve the COVID-19 problem? Work harder and smarter



Do you know people with type-O blood are more likely to be infected by norovirus? Or that West Nile virus is more likely to present in blood type A Rh(D)- individuals? Or that there is already research which suggests individuals with type-O blood are less likely to be infected by COVID-19? And if infected, their symptoms are likely to be less severe than those experienced by other ABO blood groups? Did you know these findings echo earlier research into SARS, which found that type-O individuals were less likely to be infected by the SARS virus?

Do you know young children are less likely to be infected by Helicobacter because they don’t express sufficient Leb Lewis antigen receptors, the numbers of which increase with age? Do you know sufficient levels of P(k) antigen can reduce the chance of infection by HIV-1?

Blood type, antigens, and secretor status are all important factors to consider in the spread of infectious disease. Research has shown blood type can have a significant impact on infection risk, likely severity and mortality of a disease. If you want a deeper read, see Cooling, Blood Groups in Infection and Host Susceptibility.

There is no reason to think COVID-19 will be any different from cholera, SARS, norovirus, hantavirus, chikungunya virus and so many other infectious diseases that have been shown to present different risks to people of different blood types. Would a proper understanding of that risk profile inform protective measures people should take? Would it affect who health authorities deployed in front line healthcare roles? Or how hospitals allocated protective gear during a shortage?

Blood group antigens are either sugars or proteins attached to various components in the red blood cell membrane. There are more than 340 known blood group antigens and they can be expressed at different levels within different populations. The expression of certain antigens can play a role in infection risk. 

I’m not aware of research into the susceptibility or otherwise of antigens specifically in relation to COVID-19 (the disease is too new), but it needs to be funded as a matter of urgency. If infection risk or disease severity is impacted by one or more antigens, such as the Leb Lewis antigen in the case of Helicobacter, or the P(k) antigen in the case of HIV-1, then the absence or presence of one or more antigen might explain why people within the same cohort can have very different responses to COVID-19. Specific blood antigen development might also explain why the young are generally less affected by the disease.

Research into SARS found that high levels of anti-A antibodies blocked interaction between the virus spike protein and its cellular receptor. In addition to variances in testing regimes and reported versus true infection rates, there may be other reasons we’re seeing markedly different COVID-19 mortality rates around the world. Research has shown that populations in developed countries generally have lower levels of anti-A antibodies, which could materially affect the population’s ability to fend off infection. 

A recent study of 4,850 close contacts of COVID-19 cases in Guangzhou during quarantine found 129 (2.6%) subsequently tested positive for the virus. Generally, the secondary cases were clinically milder than those of source cases and the proportion of asymptomatic and mild infections accounted for almost half of the confirmed cases among close contacts. The significant proportion of asymptomatic and mild cases, echoed in other studies (see: here, here and here),, has implications for case identification and disease control, but it is the relatively low transmission rate, echoed in an earlier serology study of SARS close contacts, and the disease profile of secondary cases that are of particular interest. 

Why isn’t there a higher infection rate among close contacts, many of whom were exposed in a household setting? The earlier SARS study found an infection rate of 0.19% among 1,068 close contacts. The Guangzhou COVID-19 study found an infection rate of 2.6%. These low figures are at odds with the generally accepted R0 of approximately 2.35. Why did the Guangzhou study find secondary infections were generally milder than primary cases?

It is possible that close contacts express a common immune response that makes them less likely to become infected, or that they suffer a less severe form of the disease if they do become infected, but such a homogenous response to a novel coronavirus within a relatively large sample size would seem unlikely. It is perhaps more likely the immune response or secretor status of the primary case plays some role in reducing transmission risk and disease severity in secondary cases. This is another area that merits urgent research.

There are so many unanswered questions about COVID-19. The British government embarked on a risky policy of herd immunity without a proper understanding of the virus or the disease it causes. As the above research demonstrates, blood group and blood antigens are likely to play a role in infection risk and disease severity. At the very least, such data would enable better modelling of the spread and impact of the disease within populations. It could assist with the identification of people who are at risk and should be offered greater protection. It might also help deploy resources more effectively to minimise infection risk and reduce transmission. 

After the SARS outbreak, a research team modelled how making use of different blood types could contribute to substantially reduce the virus transmission. If COVID-19 shares some of the same characteristics as SARS, there’s no reason a similarly sophisticated response couldn’t be used against it.

I’ve previously written for this site about some of the things the government could be doing to improve its response to COVID-19. The Prime Minister has declared war on the virus, but victory won’t be achieved in a single battle. If the close contact infection rate suggested by the above studies is anywhere near correct, the simplistic herd immunity approach still favoured by some is not a viable policy regardless of the questionable economic justifications and troubling moral issues. 

Likewise, the indefinite extension of a lockdown will cause untold economic, physical and psychological harm. It is another simplistic approach that isn’t sustainable. If we’re going to navigate our way out of this crisis in the short to medium term, in the absence of a vaccine, we’re going to have to work harder and smarter.

We need to engage this enemy on many fronts. I would suggest funding in-depth research into blood antigens and their interaction with COVID-19 will allow us to develop a key front, in addition to the test, trace, isolate strategy that has worked so well in South Korea and China. I’ve previously highlighted the need for the government to be firmer in its response to COVID-19. Its failure to provide adequate protection or testing for NHS staff is clear evidence that it has not yet risen to meet the challenge that faces us all. It must now step up.

Adam Hamdy is a novelist and screenwriter who has previously worked as a management and healthcare consultant. Follow him on Twitter: @adamhamdy