If the COVID-19 pandemic has had any effect, it is because it has allowed us all to better understand some of the actors of the immune system. Antibodies, B cells, and T cells are some of the most well-known parts of the body’s reaction. to a virus like SARS-CoV-2, but they don’t work alone.
In a paper published Aug. 18 in the journal Cell, scientists report that innate immune cells, an indispensable component of the immune formula activated to fight COVID-19, remain impaired for at least a year after infection. Those cells would possibly play a role in some of the lingering symptoms related to long COVID; More studies are needed to verify this link.
The innate immune formula is the body’s first line of defense. It is composed of general pathogen-fighting cells designed to recognize and fight all types of pathogens unexpressly, adding bacteria, viruses, fungi, and parasites (B and T cells). However, Steven Josefowicz, associate professor of pathology and laboratory medicine at Weill Cornell Medicine, and colleagues found that even the innate immune system cells retain some reminiscence of their fight against SARS-CoV-2 after a severe infection. This reminder and the reaction it generates can last at least a year after infection.
The new paper has vital implications for understanding how the immune formula (even the less expressive elements that don’t target express bacteria or viruses) is altered through infections. Understanding those alterations could also explain why other people continue to experience long-term symptoms. after facing SARS-CoV-2, Josefowicz says.
He and his team focused on the parental cells of innate immune cells, that is, bone marrow stem cells that continuously fill the source of those immune cells. Since most of those stem cells live in the bone marrow, the easiest way to access them is through bone marrow aspiration, a painful and invasive procedure in which doctors drill a component of the hip bone to reach the marrow. However, a small amount of those stem cells circulate in the blood, and Josefowicz has conducted studies not only to extract and enrich their number from blood samples, but also to verify that they constitute the same stem cells discovered in the bone marrow. This allowed him to examine those cells from patients admitted to intensive care for severe COVID-19 infections by collecting blood, which obtained bone marrow biopsies.
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Looking at these stem cells, “what becomes clear is that the immune formula is fundamentally adjusted after a severe infection like COVID-19,” he says. These cells involve genetic adjustments that modify the genes they express, prompting them to generate more inflammatory spots. . The replacement lasts at least a year after a severe COVID-19 infection, in which Josefowicz studied the cells of a few dozen patients. Because those stem cells are guilty of generating more copies of innate immune cells, the adjustments in the genes they express are passed on to the new generations of cells they produce. When he studied cells in a dish, Josefowicz discovered that they are capable of producing higher degrees of inflammatory spots and are more likely to migrate, which in a human body means they can spread. its inflammatory effects to other tissues. In animal models, those hyperreactive cells gravitate preferentially toward the lungs, brain, and heart, some of the organs hardest hit by long COVID.
A higher degree of inflammation could be a reaction to the intense effect of a severe SARS-CoV-2 infection. “A severe case of COVID-19 can also be, due to the immune formula, the beginning of a chronic infection,” says Josefowicz. , “and since the immune formula struggles to eliminate this specific pathogen, it will do everything it can to give itself a better chance of recovery.
It is not yet clear whether this memory of COVID-19 contributes to long COVID, but studies may motivate further studies to better understand how viruses like SARS-CoV-2 have effects on the immune system, either in the short or long term. “This is the beginning of a long story that will allow us to better understand how viral infections, and especially COVID-19, differ from a cold,” says Dr. Brown. Lindsay Lief, director of the medical and post-ICU ICU. . recovery clinic of Weill Cornell Medicine and New York-Presbyterian Hospital and one of the paper’s co-authors. “We want to understand how infections adjust the immune formula to have an effect not only on the symptoms you experience, but also on how you respond to your next infection or vaccination. “
The pandemic gave scientists a unique opportunity to examine how the immune formula adapts in reaction to one virus, given that many other people became inflamed at the same time and there was no vaccine to alter the immune reaction. All blood samples came from participants admitted to comprehensive care in the spring of 2020 with severe COVID-19 infections, before vaccines became available.
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As the medical records of participants who were under intensive care were available, the researchers were able to read about all the remedies they had been given and discovered a potentially useful clue about an intervention that can also mitigate the disruption of the immune system. Drugs to block IL6, which causes inflammation and increases reaction to infection, appeared to have lower levels of innate immune cells that can also produce inflammatory factors. While the drug didn’t have much effect on improving severe COVID-19 symptoms. In other people under intensive care, the study suggests it may have suppressed some of the gene expression settings in innate immune stem cells. However, this in turn can also decrease the chances of prolonged COVID-like symptoms appearing in those other people. More studies are needed to verify this theory.
“What we hope now is that others will use our approaches to link those types of adjustments to other clinical outcomes and disease states,” Josefowicz says. “Since those blood cells are more plastic than other people thought, this provides the healing option of returning them to a healthier state [after infection]. “