Needless to say there are lots of unanswered questions—or questions with a range of conflicting answers based on incomplete information or speculation—about the nature and extent of the COVID-19 virus. One of the most curious questions concerns why the virus hit some people very very hard, and others with mild or no symptoms at all. While the majority of deaths are among the elderly, there are plenty of reports of seemingly healthly younger people, and even some young healthy children, who are succumbing.
Some familiar explanations include the wide variance of the robustness of immune systems from person to person, along with underlying conditions, possible mutations of the virus, the possibility that the virus actually operates differently from pneumonia by attacking hemoglobin, and that the load or dosage of the virus individuals experience is a key variable. (Additional background on all these factors here.)
Science magazine offers another curious possibility: genetic differences. Right now this is a hypothesis only, but several studies are under way:
The projects range from ongoing studies with DNA for many thousands of participants, some now getting infected with the coronavirus, to new efforts that are collecting DNA from COVID-19 patients in hard-hit places such as Italy. The goal is to compare the DNA of people who have serious cases of COVID-19 (which stands for coronavirus disease 2019)—but no underlying disease like diabetes, heart or lung disease—with those with mild or no disease. “We see huge differences in clinical outcomes and across countries. How much of that is explained by genetic susceptibility is a very open question,” says geneticist Andrea Ganna of the University of Helsinki’s Institute for Molecular Medicine Finland (FIMM). . .
[T]here are obvious suspects, such as the gene coding for the cell surface protein angiotensin-converting enzyme 2 (ACE2), which the coronavirus uses to enter airway cells. Variations in the ACE2 gene that alter the receptor could make it easier or harder for the virus to get into cells, says immunologist Philip Murphy of the National Institute of Allergy and Infectious Diseases, whose lab identified a relatively common mutation in another human cell surface protein, CCR5, that makes some people highly resistant to HIV. . .
Other researchers working with Ganna’s initiative are recruiting COVID-19 patients directly within hospitals for such genomics studies. Italian geneticist Alessandra Renieri of the University of Siena expects at least 11 hospitals in the nation to give ethics approval for her team to collect DNA samples from willing patients. “It is my opinion that [host] genetic differences are a key factor … for susceptibility to severe acute pneumonia,” Renieri says.
Woe unto the researchers if they find any racial differences emerging from the data. The New York Times is already coiled and ready: