"Like any infectious disease, not everyone is equal in the face of Covid", summarizes French immunologist Seiamak Bahram with AFP.
The vast majority of the deaths from Covid are, therefore, elderly people.
And among the less old, hospitalizations and deaths mainly affect people at obvious risk, suffering from diabetes or other diseases.
But the inequalities go further.
"Take people of the same age, same sex, same health overall: if they are infected with a virus, here SARS-Cov-2, they can evolve in a very different way", explains Mr. Bahram.
"So, very early in the pandemic, several teams embarked on genetic predisposition."
This is the case with Mr. Bahram.
Under his leadership, researchers identified a network of genes that is associated with the development of severe forms in young and healthy patients.
They conclude, in a work published this fall, to the probable role of a gene called ADAM9.
It is one track among others.
Because, after almost two years of a pandemic, science is multiplying the genetic explanations for serious Covid.
"Research has now gathered, at an impressive speed, a mine of information on the role of hereditary genetic factors in Covid-19", underlined in October a study summarizing the main work on the subject, in the journal EBioMedicine.
The main works are twofold.
The first category compares the genomes of thousands of individuals, classified into several categories: seriously ill, mildly ill and healthy people.
By blindly crossing these data, we thus bring out more frequent elements in severe forms.
At the end of 2020, researchers thus demonstrated the presence of a particular portion of DNA, on a region of chromosome 3, in the most serious patients.
After almost two years of pandemic, science is multiplying genetic explanations for serious Covid GUILLAUME SOUVANT AFP
These results were major.
They may explain why Covid deaths are more common in populations from South Asia, in which this portion of DNA is frequently found.
Not a single gene
But the interest remains limited.
This type of study is indeed too broad to understand the mechanisms by which a specific gene can act on the disease.
In addition, they can only reveal very frequent mutations.
This is the interest of the second category of studies.
Instead of going blind, it determines from the outset which genetic mutation we will look for in patients.
It is by this track that one of the most important results in the matter was obtained.
This summer, researchers demonstrated the role of a gene, TLR7, whose mutations affect the immune response in the early stages of infection with the virus.
Researchers have demonstrated the role of a gene, TLR7, whose mutations affect the immune response in the early stages of coronavirus infection Christophe ARCHAMBAULT AFP
"We had taken genes whose mutations were already known to cause either severe influenza or diseases such as viral encephalitis", explains to AFP the French geneticist Laurent Abel, who co-directed this work published in August.
The discovery is significant because TLR7 mutations are much more common in male patients with severe forms than in the general population.
But what is the concrete interest in the fight against the disease?
Impossible, in fact, to identify in advance people at genetic risk.
"You can't test all people genetically," says Abel.
"It is not on the agenda, not feasible and not reasonable."
For the geneticist, his work allows above all "to pinpoint the circuits and pathways of the immune response which are really important".
We know that the mutation of the TLR7 gene prevents the body from reacting well to certain proteins, called interferons, which are crucial in the immune response.
This pleads for a treatment based on interferons, even if clinical trials are not yet conclusive in this regard.
In any case, we must beware of an illusory fantasy: finding the Covid-19 gene and the associated treatment.
"It would have been too simple if there was a mechanism that explained everything, that does not exist in medicine," concludes Mr. Bahram.
© 2021 AFP