What are the genetic predispositions, if any, for covid-19?

For example, https://www.express.co.uk/news/science/1258244/Coronavirus-symptoms-COVID19-susceptibility-genetic-transmission-latest-coronavirus-news mentions:

According to Dr Mirosław Kwaśniewski from the Medical University of Białystok, past studies have also found variations in the ACE2 gene are known to make people more susceptible to the coronavirus SARS-CoV. The ACE2 gene could also play a big role in SARS-CoV-2 infections.

What else is known regarding the genetic predispositions for covid-19?

I have crossposted the question at:

  • It appears to be that the type of blood (A is more likely) too Commented Apr 9, 2020 at 16:05
  • In this question Graham Chiu's answer mentions the skin color and gender too Commented Apr 9, 2020 at 16:08
  • “Higher expression of ACE2 in patients with hypertension and CVD” may make them more susceptible to SARScov2. Also the business of DVT and pulmonary embolism, high d dimmer score on admission, hypercoagulation state. May see more of a pre-existing problem with DVT among African Americans. But conclusions about COVID 19 are still pretty much preliminary and uncertain. onlinejacc.org/content/accj/early/2020/03/18/… ; blackdoctor.org/african-americans-deep-vein-thrombosis-dvt
    – Gordon
    Commented Apr 9, 2020 at 17:38
  • African Americans may have higher rates of DVT and hypertension on admission. I am just using this group as an example. Why they have a problem with both I’m sure has been studied, but whether firm conclusions can be drawn I don’t know. But the virus itself has its own innate ability it seems, to bring on hypercoagulation. So you put this together and you have a real problem. But no one is safe from this virus really until we have a vaccine since the virus here is truly a bag of “dirty tricks” we have to respect it.
    – Gordon
    Commented Apr 9, 2020 at 18:28
  • 1
    The question is unclear. Are you asking if there are genetic factors for disease severity or for catching the virus? Commented Apr 9, 2020 at 23:34

1 Answer 1


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.”



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