Coronavirus: Genes may explain why some face greater danger than others

Jack Allard, right, was a two-time All-America selection for the Bates College men’s lacrosse team before he graduated in 2016. Allard, 25, is reportedly in stable but critical condition at the Hospital at the University of Pennsylvania with COVID-19. Credit: Josh Kuckens/Bates College.

Jack Allard was the picture of health.

The 25-year-old former All-American lacrosse player was working at the Bank of America in Manhattan when he fell ill.

Days later, doctors placed Allard in a medically induced coma and on a ventilator where he remains while reportedly awaiting an experimental treatment at the Hospital of the University of Pennsylvania in Philadelphia to help him battle COVID-19.

"Jack is one of the most tenacious and gracious and humble people I’ve ever coached," said Peter Lasagna, the Bates College men’s lacrosse coach.

"He is a loved young man whom everyone is rooting for," Lasagna told Fox News on Friday.

Allard’s case is not an anomaly.

While most of the critical COVID-19 patients are elderly or have underlying medical conditions, young otherwise healthy people are also becoming severely ill – and in some cases dying – from a virus that is strangely selective and not fully understood by scientists.

Across the U.S., about 38 percent of patients requiring hospitalization due to COVID-19 are between the ages of 20 and 54, according to the Centers for Disease Control and Prevention (CDC). 

"At this moment in time, it’s a mystery why that is," said Dr. Robert Green, a professor at Harvard Medical School and a physician-scientist who directs the G2P Research Program at Brigham and Women’s Hospital and the Broad Institute.

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"While healthy young people as a group are less likely to have severe symptoms with COVID, they have to understand that some of them will become very ill and will even die from this infection," Green said. "No one should assume youth makes them invulnerable."

So why is COVID-19 – a respiratory illness never before seen in humans -- attacking certain young people with great force while sparing others?

The answers may lie in a person’s genes, according to Green.

Thousands of scientists from around the world are now pivoting to study patients’ genomes for DNA variations that might explain why some patients live and others die from the infection. Green and his colleagues at the Mass General Brigham Biobank in Boston are part of a consortium of over 100 centers and more than 300 scientists seeking to compare genetic markers to clinical outcomes among hundreds of thousands of infected patients.

"No one should assume youth makes them invulnerable"

— Dr. Robert Green, Harvard Medical School professor, physician and scientist 

One area of interest involves the ACE2 gene, which acts as a receptor to the virus – known to scientists as "SARS-CoV2."

"Mutations to the ACE2 gene might influence the ability of the virus to recognize and infect a human cell," said molecular biologist Dr. Daisy Robinton. 

The ACE2 gene encodes a receptor protein that sits on the surface of many cell types in the human body. SARS-CoV2 uses a "spike protein" to attach to this receptor, and once attached, the virus infects that cell, according to Robinton.

"ACE2 is found predominantly on human respiratory cells, which explains some of the symptoms we see including dry cough and shortness of breath," said Robinton. "However, ACE2 is also present on cells in the heart, cells of the gastrointestinal tract, and even cells that support olfaction."

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"This is partly why we see such a broad range of symptoms," she said.

According to a March 27 report in Science magazine, immunologist Dr. Philip Murphy of the National Institute of Allergy and Infectious Diseases said, "Variations in the ACE2 gene that alter the receptor could make it easier or harder for the virus to get into lung cells."

Another curious observation: Men are dying from COVID-19 at a higher rate than women, according to the data.

While there are many possible explanations for this – biological, environmental, cultural and behavioral – Green noted that the ACE2 gene is regulated differently in men than in women.

In addition to genetic variations of the ACE2 receptor, scientists are also studying whether certain blood types make a person more susceptible to serious infection from COVID-19.

Robinton, citing early medical reports on the virus, said there may be a relationship between ABO blood group and susceptibility to the disease.

"In this study of 2,173 patients in Wuhan and Shenzhen, China, people with type A blood demonstrated a significantly higher risk for acquiring COVID-19 compared with non-A blood groups, whereas people with type O blood have a significantly lower risk for infection," Robinton said.

Robinton, however, cautioned that such findings are preliminary and have yet to be replicated or to be published in a peer-reviewed journal.

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While many unknowns continue to surround COVID-19, one thing is certain: scientists everywhere are determined to fully understand the pathogenesis of the virus and all the risks factors – genetic and others – so they can develop new medications that will effectively combat the illness that has killed 17,925 people in the U.S. as of Friday afternoon.

"What is truly inspiring is that scientists around the world from every discipline are coming together in extraordinarily cooperative and creative ways," said Green.