Severe COVID-19 can lead to long-term changes in the innate immune system, the first line of defense against pathogens.
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This is evidenced by the results of a small study funded by the National Institute of Allergy and Infectious Diseases (USA).
These changes may help explain why the disease can damage so many different organs and why some people with long-term COVID have high levels of inflammation throughout their bodies.
As part of the study, scientists studied immune cells and molecules in blood samples from 38 people who were recovering from severe COVID-19 and other serious illnesses, as well as 19 healthy people. In particular, the researchers created a new technique for collecting, concentrating and characterizing very rare hematopoietic stem cells circulating in the blood.
In these rare stem cells – the parent cells of the immune system – taken from people recovering from COVID-19, scientists have found changes in the instructions that turn genes on or off. These changes were passed on to daughter cells, causing them to increase the production of immune cells called monocytes, the researchers note.
Yes, it has been found that:
- in monocytes from people who were recovering from severe COVID-19, changes in gene expression caused the cells to pump out more molecules called inflammatory cytokines than monocytes from people who were healthy or had diseases unrelated to COVID-19;
- the researchers observed these changes even a year after the participants had COVID-19.
However, due to the small number of participants in the study, scientists were unable to establish a direct link between cellular and molecular changes and health outcomes. The researchers hypothesized that the inflammatory cytokine IL-6 may play a role in setting changes in gene expression instructions, the paper notes.
The scientists tested their hypothesis both in mice with a disease similar to COVID-19 and in humans with COVID-19. In these experiments, some subjects at an early stage of the disease were injected with antibodies that prevented IL-6 from binding to cells:
- during recovery, these mice and humans had lower levels of altered instructions for stem cell gene expression, monocyte production, and inflammatory cytokines than those who did not receive antibodies;
- in addition, the lungs and brains of the antibody-treated mice had fewer monocyte-derived cells and less organ damage.
According to the scientists, the findings show that:
- the SARS-CoV-2 coronavirus can cause changes in gene expression that ultimately increase the production of inflammatory cytokines, and one type of these cytokines perpetuates the process by inducing these changes in stem cells even after the end of the disease;
- Early-acting IL-6 is likely the main driver of long-term inflammation in people with severe COVID-19.
These data shed light on the pathogenesis of SARS-CoV-2 and may provide new avenues for treatment. The results also highlight the importance of getting the recommended COVID-19 vaccines on time, which have been shown to protect against serious illness, hospitalization and death, the researchers note.
Source: Racurs
I am David Wyatt, a professional writer and journalist for Buna Times. I specialize in the world section of news coverage, where I bring to light stories and issues that affect us globally. As a graduate of Journalism, I have always had the passion to spread knowledge through writing.