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Genes, Blood Type Tied to Risk of Severe COVID-19

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SARS-CoV-2 virus particles
Caption: Micrograph of SARS-CoV-2 virus particles isolated from a patient.
Credit: National Institute of Allergy and Infectious Diseases, NIH

Many people who contract COVID-19 have only a mild illness, or sometimes no symptoms at all. But others develop respiratory failure that requires oxygen support or even a ventilator to help them recover [1]. 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 [2]. While more research is needed to pinpoint the precise underlying genes and mechanisms responsible, a recent genome-wide association (GWAS) study, just published in the New England Journal of Medicine, finds that gene variants in two regions of the human genome are associated with severe COVID-19 and correspondingly carry a greater risk of COVID-19-related death.

The two 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, the 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. The vast majority of these single “letter” nucleotide substitutions found all across the genome are of no health significance, but they can help to pinpoint the locations of gene variants that turn up more often in association with particular traits or conditions—in this case, COVID-19-related respiratory failure. 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 two places that turned up significantly more often in the individuals with severe COVID-19 than in the healthy folks. One of them is found on chromosome 3 and covers a cluster of six 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 that causes COVID-19, 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, right over the area of the genome that determines blood type. Whether you are classified as an A, B, AB, or O blood type, 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.

These findings, completed in two months under very difficult clinical conditions, clearly warrant further study to understand the implications more fully. Indeed, Franke, Karlsen, and many of their colleagues are part of the COVID-19 Host Genetics Initiative, an ongoing international collaborative effort to learn the genetic determinants of COVID-19 susceptibility, severity, and outcomes. Some NIH research groups are taking part in the initiative, and they 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.


[1] Characteristics of and important lessons from the Coronavirus Disease 2019 (COVID-19) outbreak in China: Summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention. Wu Z, McGoogan JM, et. al. 2020 Feb 24. [published online ahead of print]

[2] Genomewide association study of severe Covid-19 with respiratory failure. Ellinghaus D, Degenhardt F, et. a. NEJM. June 17, 2020.


The COVID-19 Host Genetics Initiative

Andre Franke (Christian-Albrechts-University of Kiel, Germany)

Tom Karlsen (Oslo University Hospital Rikshospitalet, Norway)

One Nation in Support of Biomedical Research?

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Graph of % change in scientific R&D spending from 2012 to 2013 in China (15%), Germany (5%), S. Korea (5%), Canada (-3%), and U.S. (15%)“It was the best of times, it was the worst of times.” Until recently, we’d never have dreamed of mentioning the famous opening line of Charles Dickens’ Tale of Two Cities in the context of U.S. biomedical research. But now those words ring all too true.

The “best of times” reflects the amazing technological advances and unprecedented scientific opportunities that exist right now. We’ve never had a better chance to make rapid progress in preventing, diagnosing, and curing human disease. But the “worst of times” is the other reality: NIH’s ability to support vital research at more than 2,500 universities and organizations across the nation is reeling from a decline in funding that threatens our health, our economy, and our standing as the world leader in biomedical innovation.

Smoking: It’s Killing Us

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Smoking harms just about every body part—from heart and lungs to bladder and blood vessels. What’s new is that smoking is more of a health hazard than we thought. Two new, NIH-funded reports make the persuasive, and alarming, case—on average, smoking takes an entire decade off of your life! But smokers take note: there are tremendous benefits from quitting, regardless of your age.

A View of the U.S. Obesity Epidemic

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Map showing Percent of Obese (BMI > 30) in U.S. Adults in 1985


Map showing Percent of Obese (BMI > 30) in U.S. Adults in 1995 by state


Map showing Percent of Obese (BMI > 30) in U.S. Adults in 2005 by state


Map showing Percent of Obese (BMI > 30) in U.S. Adults in 2010 by state

These snapshots reveal a very disturbing trend: the rise in obesity in the US from 1985 to 2010. Today one third of adults in the US are obese, another third are overweight.

Because obesity has risen to epidemic levels—causing devastating and costly health problems, reducing life expectancy, and provoking stigma and discrimination—the NIH has established the NIH Obesity Research Task Force to accelerate progress in obesity research. For example, why are some individuals more susceptible to obesity? Can knowledge of biology and behavior be leveraged to develop better intervention strategies? What strategies work? For whom? Can these approaches be scaled up?