[Article published today in the Diario de La Rioja today about the type of tests we are going to perform to find out the DNA changes that contribute to the susceptibility to severe COVID-19 symptoms.]
Sometimes I think about how to explain genetic susceptibility to severe COVID-19 symptoms without using technical vocabulary. In the lines that follow, I will try to explain how to find genetic factors that contribute to severe symptoms in COVID-19, and why it is important to do so. It doesn’t help that everything in genetics today is computer-based. Nor is it that, despite having a map of all genes (the human genome), each person has a different version of each gene (there are about 20,000 genes in total). It is precisely some of these genes, all of them present in each cell, that determine our susceptibility to severe COVID-19 symptoms. Serious symptoms that can be traced directly to a sequence of DNA variations. A sequence capable, for example, of dictating the instructions of how to build a receptor with which the virus infects human cells.
It would be great to be able to say that a DNA variation is the cause of more or less severity. However, it cannot always be done. Of all the possible combinations, only a few variations will contribute to the desired effect. This is the typical problem of genetics: differentiating “causal variations” from “natural variations”. There is no way we can find needles in such a large haystack unless we manage to have a sufficient number of patients, and compare their millions of variations with those of infected people who have no symptoms. Variations that are different and that appear only in severe patients will be those that become candidates for further study.
After studying each of the candidate variations, we then select those that help to predict the effect of severe symptoms in a patient. That’s how, without getting too into the scientific jargon, how we are working to find genetic conditioning factors for severity in COVID-19. There is no way to do this without using a data infrastructure advanced enough to analyze millions of genetic variations in many patients. However, and as complicated as it may seem, what is complex is not the data analysis itself, but rather finding and characterizing so many severe patients as to sufficiently discriminate the genetic variations that contribute to severe symptoms. Only then, with millions of data points per patient, will we find those tiny DNA changes that may help create new predictive tools against the pandemic. Tools capable of identifying those who are most at risk of being seriously affected (before they become infected) given their susceptible gene.