The Corner

Health Care

How Much Does Genetics Explain Who Can Fight Off a Coronavirus Infection?

A taxi driver wears face mask at the Nima market, as Ghana lifts partial lockdown amid the spread of the coronavirus disease (COVID-19), in Accra, Ghana April 20, 2020. Picture taken April 20, 2020. (REUTERS/Francis Kokoroko)

A new study of groups of coronavirus patients in New York state sorted by race concluded whites were the least infected, with the fewest hospitalizations and deaths. While Hispanics had the most infections and the lowest rate of diagnoses, Blacks were most likely to be hospitalized or killed by the coronavirus.

When all is said and done about the pandemic of SARS-CoV-2, I suspect we will learn that patients’ genetics played a significant role in whether their body managed to fight off the virus. There are just so many surprising examples of elderly patients who manage to fight it off while much younger and seemingly much healthier patients — including doctors and nurses — succumb to the virus.

Research into human genetics has unveiled some fascinating and downright bizarre disparities in the ability to fight off pathogens.

Back in 2012, a study of human cells’ ability to resist anthrax bacteria selected cells from 234 individuals from four locations — Nigeria, Tokyo, Beijing, and “Utah residents with ancestry from northern and Western Europe.” Three of the individuals with European ancestry “showed extraordinary resistance to toxin lethality” — about 30,000 times more resistant to anthrax than the least-resistant cells in the sample. Removing the three outliers still left the scientists with a wide range in resistance, with the next most resistant cells about 250 times more resistant than the least. The study confirmed that these sample donors were family and that the resistance was an inherited trait. In short, some unspecified genetic line of European heritage is, if not immune to anthrax, much more resistant to it than other groups.

Then there is the example of the Tharu people, in the region around the Indian–Nepalese border. A region of Nepal called Terai was infested with mosquitos and had high rates of malarial infections — but the local Tharu were either unaffected or minimally effected; they effectively had a genetic immunity to malaria — and the prevalence of malaria offered the Tharu a de facto defense against invaders. (The program for malaria control that started in the region in the 1950s did not work out well for them.)

Back in 2016, researchers at the University of Montreal concluded that Americans of African descent have a stronger immune response to infection compared to Americans of European descent. They emphasize “stronger” rather than “better” because an immune system that reacts more strongly can create its own problems; if your body’s immune system reacts too much and it starts attacking healthy cells, you could develop an autoimmune disease like rheumatoid arthritis or lupus or Crohn’s disease or multiple sclerosis. In fact, one of the potential effects of a coronavirus infection is a “cytokine storm,” where the immune system goes into overdrive and starts attacking healthy cells and disrupting other needed operations of the body. If African Americans are already more likely to have a strongly reactive immune system, and then the coronavirus triggers a cytokine storm . . . this could well be a factor in the higher mortality rate among this population.

Do systemic inequalities in society contribute to the higher death rate among Hispanics and Blacks in New York state? Almost certainly. If you’re poor and not seeing a doctor regularly, your health is extremely likely to suffer — problems go unrecognized, undiagnosed, and untreated.

But we’re all walking around with genes, inherited from our parents, that make us more resistant to some threatening pathogens and more vulnerable to others. When we see some people whom we would have thought could have survived the coronavirus succumb to it, and some people who looked like they had no chance managing to make a full recovery . . . how much of the answer can be found in patients’ genes?

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