Despite its ability to spread quickly, COVID-19 seems to be selective in terms of severity. Many of those who have contracted the virus do not show severe symptoms and the majority of critically-ill patients already have complications like heart disease and diabetes. However, some of the deceased were previously healthy and even relatively young. What factors lead to such a varied response? It is an important question for scientists who are now looking at the genetic architecture of the affected individuals.
Scientists aim to collect DNA samples from thousands of participants that have suffered from COVID-19. Their objective is to compare the DNA of people who had severe cases of COVID-19 with no chronic diseases (such as heart disease, diabetes or lung disease) with those that have mild disease or no disease at all.
Geneticist Andrea Ganna of the University of Helsinki’s Institute for Molecular Medicine (FIMM) and FIMM’s director Mark Dally have taken the lead and have also created a website for the project. “We see huge differences in clinical outcomes and across countries. How much of that is explained by genetic susceptibility is a very open question,” said Ganna.
It is difficult to say what the outcome of the gene hunt will be in this early phase, but there seems to be a suspect – the gene that code the angiotensin-converting enzyme (ACE 2). The angiotensin converting enzyme is a cell surface protein present in the human body which acts as a receptor for the coronavirus. The ACE2 present on the surface of the cells is used by the virus to make its entry into the airway cells. Variation in ACE 2 receptor caused by the variation in the gene encoding it could make the virus’ entry to the human cell easier or harder. For example, the CCR5 is a human cell surface protein that the HIV virus uses to get into the body. There are relatively common mutations in the gene that encodes CCR5 and as a result some people develop high resistance to HIV. It was a remarkable finding by the lab led by Philip Murphy of the National Institute of Allergy and Infectious Diseases, US.
The strategy that Ganna and his team has adopted is to collaborate with biobanks that collect thousands of volunteers’ DNA, and look for the link between their health and their DNAs. For now, at least a dozen biobanks have reportedlyagreed to contribute COVID-19 data from participants who have agreed to it. Most bio-banks are based in Europe and the US. The important biobanks that have agreed to collaborate are Finngen, the Biobank repository of the Finnish population; Biobank of Icahn School of Medicine at Mount Sinai, US; UK Biobank, one of the world’s largest Biobanks and Harvard University’s Personal Genome Project.
Other researchers collaborating with Ganna’s team are collecting genetic information of COVID-19 patients directly from hospitals. Alessandra Renieri, an Italian geneticist from the University of Siena expects that Italy’s 11 hospitals will provide approval to collect genetic samples from willing patients.
Some researchers are also planning to see if the human blood group has to do anything with coronavirus resistance. Recently, a Chinese team reported that people from the O blood group may be protected from the virus. To study this, researchers plan on analysing whether difference in Human Leukocyte Antigen genes can be a factor in disease resistance. The Human Leukocyte Antigens influence the immune system’s response to bacteria and viruses.