“As with any other genetic disease, not everyone is the same when faced with the Covid virus,” French immunologist Siamak Bahram explains to AFP.
The vast majority of people who die of greed are old people. Those who are severely affected and younger suffer from other problems such as obesity or diabetes.
But researchers also examine those who do not present any a priori risk profile.
Under the supervision of Dr. Bahram, a group of researchers has identified a series of genes associated with the emergence of severe forms of the coronavirus.
They are young patients who do not have health problems. The team has just published a study in which they point to the potential role of a single gene, ADAM9. One guide among many others.
“Research has collected a huge amount of information about the role of genetic factors in the COVID-19 virus with astonishing speed,” another study summarizing key work on the topic was highlighted in October in the journal EBioMedicine.
– Two types of search –
The main searches are of two types.
The first category compares the genomes of thousands of individuals, categorized into several categories: severely ill, moderate, and healthy.
Random crossover of the data reveals frequent elements between severe forms of covid-19.
In late 2020, it was discovered, for example, that there are critically ill patients with COVID-19 who have a specific piece of DNA in a region of chromosome 3.
This piece of DNA appears in particular in some populations in South Asia, which explains the more frequent deaths from coronavirus in that region.
– No h frmula mgica –
But at the moment, these types of data crossings are very vast. It was not possible to understand why the gene needed to act on disease. Moreover, these analyzes only reveal very common genetic mutations.
Which falls into the second category of studies. Rather than starting at random, these studies choose a specific genetic mutation and start from it.
This path gave one of the most important results in this topic. The TLR7 gene, whose mutations affect the primary immune response to infection.
“We chose genes whose mutation we knew caused severe influenza or diseases such as viral encephalitis,” said French geneticist Laurent Appel, co-director of the study published in August.
This finding is significant because TLR7 mutations appear more frequently in male patients who have become seriously ill with coronavirus, compared to the rest of the population.
But what is the specific benefit of all this in fighting disease?
It is impossible to identify people at genetic risk before they become ill. “You can’t control them all from a genetic point of view,” Abel says. “This is neither possible nor reasonable.”
The geneticist explained what this research allows “to emphasize the circuits and pathways of the immune response that are really important.”
The TLR7 gene mutation is known to prevent the body from responding properly to certain proteins, interferon, which are critical to the immune response.
For this reason, the study suggests an antiviral treatment based on interferon, although clinical trials have not been favorable so far.
In any case, there should be no illusions about the presence of a single gene that predisposes to covid-19.
Bahram concludes, “It would be very easy if there was a mechanism that explains everything that is not found in medicine.”
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