- Several studies have found that for Covid-19, like Sras and Mers, some patients do not die from the infection, but from an exaggerated reaction from their immune system.
- We call this runaway "cytokine storm" and the phenomenon is of great interest to researchers.
- If we succeeded in limiting the action of these cytokines, without suppressing the immune reaction, we could certainly save more serious patients from the coronavirus.
One of the anxieties about this new coronavirus is that a patient's condition can suddenly deteriorate. If in four out of five cases, this Covid-19 results in mild symptoms, in 10 to 15% of cases, the patient finds himself in respiratory distress with the need for artificial ventilation and a respirator. If this new disease still keeps a lot of gray areas, a working hypothesis is of increasing interest to researchers on these serious cases: that of a "cytokine storm".
What is the "cytokine storm"?
Cytokines are substances naturally produced by cells of the immune system to promote the inflammatory reaction and thus defend the attacked body. "The molecules that attract immune cells are cytokines," explains Morgane Bomsel, immunologist and research director at CNRS. After a short week, some patients end up with an acute respiratory syndrome. This medical condition has been correlated with the detection in plasma of a large amount of these cytokines. That's why we call it a "Cytokine storm": these molecules are secreted in too large a quantity. This runaway can become fatal. "In some individuals, the reaction gets carried away to the point of destroying tissues and organs such as the heart, the kidney," adds Frédéric Altare, research director at Inserm and immunologist. Instead of protecting the body from infection, it turns on itself. As in autoimmune diseases.
Not specific to Covid-19
This phenomenon of “hyper-inflammatory storm” has been identified and described for only twenty years. He was singled out to explain the danger of two other respiratory diseases caused by coronaviruses, SARS (774 died mainly in Asia in 2002-03) and Mers (Middle East respiratory syndrome, 866 deaths since 2012). Two coronaviruses that are similar, at least in some features, to Covid-19.
"Evidence is accumulating to suggest that some of the patients suffering from severe forms of Covid-19 are subject to cytokinic shock syndrome" writes, with British colleagues, Jessica Manson, specialist in inflammatory phenomena at University College Hospital from London, in the medical journal The Lancet from March 16. "It's likely," says Frédéric Altare. But this counterproductive reaction does not occur in all cases, even severe, of this new coronavirus. "That would only explain part of the deaths," he says. For SARS, it was found that around 50% of deaths were linked to this overreaction. "
Why do some patients succumb to it and not others? Researchers do not yet have the answer. "It would seem that the immune system must be active enough to observe this storm," says Morgane Bomsel, who works at Cochin Hospital to better understand these "cytokine storms". And that it is therefore less present, "in children, because the immune system is too immature and in the elderly, because it is deficient".
An interesting track
Why does this hypothesis fascinate researchers? “It would be a priority to find a way to stop the runaway which risks killing the patient faster than lung infection, answers Frédéric Altare. How? 'Or' What ? "We think that if we blocked the interaction between the cytokine and its receptor, we would avoid this runaway," says Morgane Bomsel. Who uses this image: “if you pour water on sugar, it will melt, but if you put a plastic sheet, you prevent the water from destroying this sugar. »It is still necessary to determine which cytokine inhibitor to activate and to what dose we must limit this reaction. "This inflammatory response is beneficial to the patient," recalls Frédéric Altare. If this reaction is blocked, the patient can no longer fight the virus and he dies of viral infection. This is also why people with mild symptoms were advised not to take anti-inflammatory drugs. "
Meticulous research work. “There are dozens of molecules produced for immunity. And in general, we do not ask ourselves the question of sorting them [between those effective and those dangerous]. Except from SARS and the Seas, but we had very few patients and quite a few reliable data. "
The good news is that we are not starting from scratch, since some of these inhibitors already exist on the market and Chinese studies have already looked into the matter. "We will be able to rely on this first sorting among the inhibitors carried out in China", welcomes Frédéric Altare. Several clinical trials have been launched in Denmark, China, the United States and Italy to test the effectiveness of molecules (notably letocilizumab and sarilumab) that block the reception of certain cytokines, as detailed in this article from Vidal. In France, the Necker hospital launched a therapeutic trial on 240 patients on March 27 which should determine by December whether taking sarilumab improves the patients' condition. One among others, assures Frédéric Altare, since researchers working on transplants and immunotherapy also see these immunity over-reactions.
"There are exciting things about treatments in many directions," says Morgane Bomsel. But you have to check these assumptions and it takes time. "
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