A more severe form of COVID-19 results in the death of an even higher number of T cells, which opens the door to a worsening of the disease. (Photo: The Canadian Press)
The coronavirus incites certain immune cells that would normally fight it to commit suicide instead, researchers at Laval University have found, which allows the disease to then take on even greater proportions.
A kind of vicious circle then sets in: a more serious form of COVID-19 leads to the death of an even higher number of T lymphocytes, which opens the door to a worsening of the disease.
“The status of patients is associated with more or less significant cell death and the greater it is, the more, it seems, that it is associated with the severity of the disease”, summed up Professor Jérôme Estaquier, from the Faculty of Medicine of Université Laval and the Research Center of the CHU de Québec-Université Laval.
Two-thirds of patients hospitalized with COVID-19 have abnormally low levels of lymphocytes, which play a central role in the immune response against infections.
By studying 41 people admitted to hospital with COVID-19, including 11 who had to be transferred to intensive care, Professor Estaquier and his colleagues found that these patients presented with an immune deficiency when they presented to the hospital. hospital, and that the extent of this deficit was related to the severity of the disease.
SARS-CoV-2 infection leads to increased blood levels of a protein called FasL. When it binds to a receptor on the surface of T lymphocytes, it triggers a form of cell suicide called apoptosis. The higher the levels of FasL, the greater the mortality of lymphocytes.
With 30 years of work against AIDS, Professor Estaquier quickly noticed commonalities between the two health problems.
“There was a certain similarity between this early deficit that we observed in COVID patients and what we had as knowledge in the context of AIDS,” he explained.
A similar process of programmed cell death of lymphocytes is thus seen in AIDS patients. In both cases, infected people struggle to generate a robust immune response to the virus. If too many lymphocytes fall in battle, the disease is likely to take over.
And while AIDS and COVID-19 may seem like distant cousins at first glance, many infectious diseases have one thing in common: they first drive the immune cells that are meant to destroy them to suicide, notes Professor Estaquier.
The work of the AIDS researcher’s team, however, gives us a head start on the coronavirus. Experiments carried out in the laboratory have thus demonstrated that it may be possible to considerably reduce lymphocyte apoptosis.
“We think that indeed there could be applications that could be important, even for people who are hospitalized with a severe form of the disease,” he said.
There could also possibly be implications for associated pathologies such as the long form of COVID, the causes of which remain unclear, but for which “one could now wonder if it is not a problem of early immune deficiency that these people have eu”, added Professor Estaquier.
Details of this discovery are published by the scientific journal Cell Death & Differentiation.