The after-effects associated with long-term COVID could result from the death, during the acute phase of infection, of certain cells of the immune system, a Franco-Quebec research team has found.
This discovery could potentially make it possible to identify, from a simple blood test, patients hospitalized for COVID-19 who are more likely to develop long-term COVID, and therefore to treat them more quickly.
“We want to be able to predict better in order to have better care,” the co-director of this study, Professor Jérôme Estaquier of the Faculty of Medicine at Laval University, explained to The Canadian Press.
Professor Estaquier and his colleagues thus discovered that certain cells of the immune system, T4 lymphocytes, show significantly higher rates of cell death in patients who will have long COVID than in patients who will recover without after-effects.
This discovery comes from the study of 29 people treated for COVID-19 at the University Hospital of Nîmes, France. In the months following hospitalization, nineteen patients suffered from long-term COVID, while the other ten had no after-effects.
The researchers found that the percentage of T4 lymphocytes engaged in a form of programmed cell death (apoptosis) was 37% in the long COVID group and 24% in the other group. By way of comparison, in healthy subjects, the percentage of T4 lymphocytes undergoing apoptosis is approximately 20%; this percentage is comparable to that of patients who have recovered well from their infection, but it is almost half that of patients who have had after-effects.
“The level of cell death of these cells, therefore the loss of these lymphocytes, is associated with an evolution which has been maintained over time, that is to say with attacks and anomalies […] clinics,” summarized Mr. Estaquier, who is also a researcher at the Research Center of the CHU de Québec-Université Laval.
Researchers are currently unable to explain why T4 lymphocyte apoptosis is greater in certain individuals than in others. However, they found that it is more common in women than in men, which raises the hypothesis of hormonal factors.
A similar phenomenon had also been observed for AIDS, said Professor Estaquier, since “the clinical evolution is proportional to this loss of lymphocytes. The more significant these damages are, the more rapid the progression towards the disease will be.”
In the case of SARS-CoV-2, this immunosuppression could allow the virus to disseminate more easily and survive in certain parts of the body, notably in the intestinal mucosa, researchers believe. It could also promote the reactivation of latent viruses or even disrupt the body’s defense mechanisms.
The fall of these “first defense barriers”, said Professor Estaquier, could therefore favor the establishment of the virus.
“There are fewer good quality antibodies, and as a result the virus is probably less controlled,” he said. And since it is less controlled, well that actually allows it to perhaps reach particular tissues or tissue niches, and therefore perhaps to establish itself more permanently. Perhaps this is actually what causes the complications we see. There is also a certain amount of work that suggests the virus lasts longer. »
Researchers have identified a molecule, Q-VD, which is able to reduce the apoptosis of T4 lymphocytes by 60% during laboratory experiments, but we are still very far from use in humans.
Instead, they will now seek to check the rate of apoptosis of these lymphocytes in people who suffer from long-term COVID. If this rate is still high several months after infection, this would support their hypothesis, which could restart the search for drugs to prevent apoptosis of these cells.
“There are manifestations at the clinical level that suggest that the immune system is not as able to defend itself […]which could explain the complications that we observe,” concluded Professor Estaquier.
The findings of this study were published by the medical journal Frontiers in Immunology.