Indirectly, of course, the genetic backgrounds of underlying diseases and conditions (such as obesity) that predispose to a severe course of Covid-19 (such as obesity) should also be included, but there also appear to be much more direct links.
The fundamental mystery of the coronavirus epidemic is well known to everyone: About eighty percent of infected people produce asymptomatic or mild symptoms, and the virus survived people between the ages of 108, 113 and 116 years old. While healthy young people can die. Early research naturally focused on the course of the disease, the ways the virus spreads, and the genetic features of the pathogen, but over time it has become apparent that genetic testing of patients is inevitable as well.
At the start of the epidemic, three Iranian brothers died around the same time. They lived separately from each other, none of them had chronic disease, while the vast majority of those infected locally did not get sick (as elsewhere). As early as April 2020, an Iranian study described the condition as a virus
Which, according to the authors, indicates some type of genetic predisposition.
A coordinated search has begun
Because collecting and analyzing such genetic samples takes many people and hours of work, universities, research institutes and hospitals around the world have teamed up. It is important to obtain genetic samples from all continents so that something that is actually unique to a major race or ethnicity does not seem universal.
There are two basic types of collaboration models.
In one, partners were sought to prove specific research assumptions so that they could work faster. This is Covid human genetic effort An international project called India, which brings together experts on the subject from India to Brazil and Switzerland to Japan. Here, an attempt is being made to determine the genetic basis for an individual’s susceptibility to natural resistance to the virus – based on a coordinated methodology.
Another way to communicate globally is to organize relevant human genetic research on one common platform, whether continuous or closed. This was launched in March of last year Covid-19 Host Genetics Initiative, Which gathers the work of more than 2000 scientists from 54 countries. Their website currently contains 158 studies available from around the world.
Evidence already exists
We don’t yet know what it depends on who runs the virus almost unnoticed and who gets seriously ill, sometimes in the ICU. However, all researchers agree that there is not a single gene that explains all this, but the combined effect of several factors. Two of these have already been identified.
The Leipzig Institute reported last fall that one in six Europeans has a section of chromosome 3 that triples the odds of being on a ventilator. On chromosome 12, on the other hand, there is a set of genes that reduce the fear of someone falling into the ICU by roughly a fifth – and this variant is present in half of Europeans. (Both copies were inherited from our Neanderthal ancestors anyway.)
Another group of patients compared patients’ DNA from more than 200 ICUs with the genomes of a healthy population and found that there are rare variants of TYK2 (and in some cases DPP9 and CCR2, which stimulate the action of immune cells).
It makes the body’s self-defense system “angry” by actually causing massive damage to the lungs.
Then there is a slower-than-normal immune interferon. These proteins fail to stimulate the body’s immune response to a Covid infection in a timely manner, which is why irreversible conditions often arise. This is caused by an incomplete gene variant (IFNAR2), for example, which some experts say is responsible for the tragedy of nearly 15 percent in intensive care, while others say only 4 percent – but everyone acknowledges the phenomenon. Plus the fact that if a person had the genetic variant in question, it would increase the likelihood that the infection would be severe in him by about a third.
A similar study found that a very rare gene mutation (TLR7) may also play a role in the development of severe disease in men under the age of 60. Although this tiny immune defect is responsible for only two percent of cases, it can sometimes explain why a man in his 80s would survive what a 20-year-old might not be able to do.
An Austrian study, which compared mild to severe patients, found that those with partial or complete deficiency of a specific natural killer cell (NKG2C) receptor in the body were more likely to be ventilated. Roughly a third of people have fewer of these and 4 percent of the population do not find them at all.
Lab tests are underway, and of course the picture is far from complete. However, researchers are confident that a deeper understanding of human genetics could also give a new impetus to developing drugs against the Coronavirus.
(Cover photo: L.
Processing coronavirus samples with a laboratory pipette at Biogroup’s laboratory, West London, January 21, 2021.
Photo: Justin Thales / AFP)
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