Blood Type Tied to Risk of Severe COVID-19 Disease

Many people who contract the SARS-CoV-2 coronavirus have only a mild illness, or sometimes no symptoms at all.

But many others develop respiratory failure requiring oxygen support or even a ventilator to help them recover, stated Dr. Francis S. Collins, in the National Institutes of Health (NIH) Director’s Blog, posted on June 18, 2020.

Excerpts from Dr. Collins weekly blog continue below:

It’s clear that this happens more often in men than in women, as well as in people who are older or who have chronic health conditions.

But why does respiratory failure also sometimes occur in people who are young and seemingly healthy?

A new study suggests that part of the answer to this question may be found in the genes that each one of us carries.

A genome-wide association (GWAS) study, just published in the New England Journal of Medicine on June 17, 2020, finds that gene variants in 2 regions of the human genome are associated with severe COVID-19 disease and correspondingly carry a greater fatality risk.

These stretches of DNA implicated as harboring risks for severe COVID-19 are known to carry some intriguing genes, including one that determines blood type and others that play various roles in the immune system.

In fact, this study’s findings suggest that people with blood type A face a 50 percent greater risk of needing oxygen support or a ventilator should they become infected with the novel coronavirus.

In contrast, people with blood type O appear to have about a 50 percent reduced risk of severe COVID-19.

These new findings—the first to identify statistically significant susceptibility genes for the severity of COVID-19—come from a large research effort led by Andre Franke, a scientist at Christian-Albrecht-University, Kiel, Germany, along with Tom Karlsen, Oslo University Hospital Rikshospitalet, Norway.

Their study included 1,980 people undergoing treatment for severe COVID-19 and respiratory failure at seven medical centers in Italy and Spain.

In search of gene variants that might play a role in the severe illness, the team analyzed patient genome data for more than 8.5 million so-called single-nucleotide polymorphisms, or SNPs.

To find them, the researchers compared SNPs in people with severe COVID-19 to those in more than 1,200 healthy blood donors from the same population groups.

The analysis identified 2 places that turned up significantly more often in individuals with severe COVID-19 than in healthy people.

One of them is found on chromosome 3 and covers a cluster of 6 genes with potentially relevant functions.

For instance, this portion of the genome encodes a transporter protein known to interact with angiotensin-converting enzyme 2 (ACE2), the surface receptor that allows the novel coronavirus SARS-CoV-2 to bind to and infect human cells.

It also encodes a collection of chemokine receptors, which play a role in the immune response in the airways of our lungs.

The other association signal popped up on chromosome 9, called locus 9q34.2, right over the area of the genome that determines blood type.

Whether you are classified as an A, B, AB, or O blood type, it depends on how your genes instruct your blood cells to produce (or not produce) a certain set of proteins.

The researchers did find evidence suggesting a relationship between blood type and COVID-19 risk.

They noted that this area also includes a genetic variant associated with increased levels of interleukin-6, which plays a role in inflammation and may have implications for COVID-19 as well.

Some NIH research groups have recently launched a study to look for informative gene variants in 5,000 COVID-19 patients in the United States and Canada.

The hope is that these and other findings yet to come will point the way to a more thorough understanding of the biology of COVID-19.

They also suggest that a genetic test and a person’s blood type might provide useful tools for identifying those who may be at greater risk of serious illness, concluded Dr. Collins’s weekly blog.

Dr. Collins was sworn in on August 17, 2009, as the 16th director of the NIH.

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