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If you’ve never had COVID, should you relax or worry?


Genetic protection?

A new study in Nature Genetics explains a potential genetic relationship. Study authors found evidence that levels of expression of angiotensin-converting enzyme 2 (ACE2) – which helps regulate blood pressure, wound healing, and inflammation, but has also been shown to serve as an entry point into cells for some coronaviruses like SARS-CoV-2 — influence COVID-19 risk.

Manuel A. Ferreira, PhD, an executive director for analytic genetics at Regeneron Pharmaceuticals, said in an interview that ACE2 receptors — what he calls the “gateways” for SARS-CoV-2 to enter the body — are different in people who have inherited a particular allele.

The researchers have found that that allele is associated with lower risk of SARS-CoV-2 infection.

“It’s quite substantial -- a 40% risk reduction if you carry the allele that reduces ACE2 expression,” he said. They were not able to discern from this study, however, whether that could predict severity of disease.

The team also looked at a series of six genetic variants elsewhere in the genome and developed a risk score to see if it was possible to predict who might be more susceptible to severe COVID.

Dr. Ferreira said the score only slightly improved predictive abilities beyond factors such as age, sex, weight, and comorbidities. Further information will help hone the ability to predict the likelihood of developing severe disease on the basis of genetics, Ferreira said.

“As we identify more genetic risk factors for COVID — variants like the ACE2 variant that will affect your risk of having COVID — the more informative the risk score will be,” he said.

Several authors of the Nature Genetics article are current and/or former employees of AncestryDNA and may hold equity in AncestryDNA. Several are Regeneron employees and/or hold stock in the company. Dr. Ferreira is an employee of Regeneron and holds stock in the company. Dr. Schaffner and Dr. Adalja report no relevant financial relationships.

A version of this article first appeared on


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