They are young, healthy and still die from Kovid-19 or are in hospital. These rare cases testify to an invisible risk, but researchers understand more: genetic predisposition
“Like any infectious disease, not everyone is the same on the face of a cowboy,” summarizes the French immunologist Siamese Bahram. Hence the vast majority of Kovid deaths are elderly.
And in the younger generation, hospitalizations and deaths mainly affect people at apparent risk of developing diabetes or other illnesses. But the inequalities go further.
Everyone is worried
“Take people of the same age, the same gender, the same health overall: if they were infected with the virus here SARS-Cov-2, they would develop in a very different way. So, at the very beginning of the epidemic, many teams embarked on genetic predisposition,” he said.
This is the case of Siamese Bahram. Under his leadership, researchers have identified a network of genes involved in the development of acute forms in young and healthy patients. In a work published this fall, they concluded the potential role of a gene called ADAM9.
These results are key. They can explain why Kovid deaths are so high in the population of South Asia, this piece of DNA is often found.
There is not a single gene
But the interest is limited. This type of study is actually quite extensive to understand the mechanisms that work on a particular genetic disease. In addition, they can very often only reveal mutations.
This is of interest to second class studies. Instead of blindness, it determines from the beginning what genetic mutation we look for in patients.
One of the most important results in this regard was obtained by this track. This summer, researchers demonstrated the role of a gene called TLR7, whose mutations affect the immune response in the early stages of infection with the virus.
“We took the genes, whose mutations are already known to cause diseases such as acute influenza or viral encephalitis,” explained Laurent Abel, a French geneticist who co-directed the work, which was published in August.
This finding is important because TLR7 mutations are more common in male patients with more severe forms than in the general population. But what is the concrete interest in the fight against disease? It is impossible to identify people with a genetic risk in advance.
“We can not genetically test all people,” Laurent Abel stressed. “It is not on the agenda, it is not feasible and it is not reasonable. “For the geneticist, his work is, above all,” that allows us to identify circuits and really important immune response pathways.
In any case, we must be wary of an illusory hypothesis: the discovery of the Kovid-19 gene and the treatment associated with it. “It would have been much simpler if there had been a mechanism to explain everything that is not in medicine,” Siamak Bahram concluded.