The only data we have suggesting a genetic resistance to Covid-19 so far is that blood group O is protective and so is being female. The latter may relate to the numbers of ACE2 receptors since the virus uses this as one of its 4 attack points, and ACE2 is encoded on the X chromosome giving women more ACE2 receptors. Blood group O may confer resistance too because these people may have some anti-A antibodies which may interfere with the binding of the SARS-CoV-2 to the ACE2 receptor.
Although black people have been reported to have much higher rates of fatality than others this may be instead related to the existence of co-morbid conditions such as diabetes, hypertension and renal diseases. And the same applies to Hispanics who represent the majority of deaths in NY city (according to Surgeon General Jerome Adams 11th April 2020).
23andme are conducting research to see if there is a genetic predisposition
If the company collects enough responses from people who’ve contracted Covid-19, 23andMe’s research team will conduct a statistical analysis called a GWAS, or genome-wide association study. A mainstay of genetic research, GWAS involves sorting people into different groups—in this case probably based on symptoms—and scanning their DNA data to see if certain single-letter variations in the genetic code show up more often among people with certain symptoms. If that happens a significant number of times, they can say with some confidence that those variants are linked to those symptoms.
but such scans are helpful really when picking up common variants, and not rare ones
But it’s these very rare mutations that are likely driving cases of extreme susceptibility to Covid-19, says Stephen Chapman, a respiratory physician and researcher at the University of Oxford’s Wellcome Trust Centre for Human Genetics, who isn’t part of the 23andMe project. In the mid-2000s, he conducted some of the first genetic studies on susceptibility to bacterial pneumonia, and discovered rare mutations in immune-related genes that made otherwise healthy children and adults especially susceptible to an invasion by one particular bacteria. Chapman suspects similarly rare mutations involved in immune function or inflammatory responses could be what’s putting young, apparently fit adults without other risk factors into ICU beds. “This is the major drawback of GWAS, in my view,” he says. “It will miss those rare, causative mutations.”