Scientists have discovered the trigger that does inflammation spirals out of control for some children after a COVID-19 infection.
It turns out that the immune system mistakes a protein made in most parts of the body as foreign because it mimics what is part of SARS-CoV-2, the virus that causes COVID 19.
The condition, called multisystem inflammatory syndrome in children (MIS-C), was was first identified early in the pandemic in a small percentage of children who recovered from COVID-19.
Many of these children were initially asymptomatic during a period of viral infection but, two to six weeks later, developed life-threatening inflammation in the heart, brain, skin, blood or digestive system.
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MIS-C always comes with feverbut it can also cause weakness, dizziness, stomach pain or rash.
Until recently, scientists weren’t sure exactly how COVID-19 and MIS-C were connected or why the immune system might turn on in the body after an infection. To understand what drives inflammation in MIS-C, researchers profiled the immune systems of 199 children with MIS-C and 45 who recovered without developing the condition.
The study, published Aug. 7 in the journal Naturediscovered 30 autoantibodies—antibodies that target a person’s own body instead of a foreign invader—that were present in patients with MIS-C but not in those without the condition.
The autoantibodies with the strongest profile targeted a protein called SNX8, which is found in almost every part of the body because of its role in classification and transport of molecules inside the cells.
It turned out that part of the “nucleocapsid protein” of the coronavirus closely resembles the part of SNX8 that is targeted by these autoantibodies. The nucleocapsid protein is part of the outer layer of the virus, which envelops its genetic material. This similarity raised the possibility that, in some patients, the immune system was mistaking SNX8 for its SARS-CoV-2 counterpart and, therefore, attacking tissues that expressed it.
To support this theory, the team studied T cells, which recognize and kill virus-infected cells in the body, from patients with and without MIS-C. Only T cells from MIS-C patients reacted to SARS-CoV-2 and SNX8, supporting the mistaken identity hypothesis. The discovery could provide new approaches to diagnosing the ongoing condition.
However, SNX8 is unlikely to be the whole story behind MIS-C.
“We believe that a number of rare factors come together to allow someone to get MIS-C,” senior author Joseph DeRisia professor of biochemistry and biophysics at the University of California, San Francisco (UCSF), told Live Science. “The bodies are a part of that, but not the only part.”
Either way, MIS-C is much less of a problem than it used to be.
“The fascinating thing is that MIS-C has largely disappeared, except for children who are unvaccinated or whose vaccines have faded,” he said. Dr. Aaron Bodanskyfirst author of the study and a pediatric critical care fellow at UCSF. “If you predispose the immune system [to SARS-CoV-2] by being vaccinated, there won’t be as much time to develop this unusual response.”
However, declining vaccination rates with new, updated vaccines for COVID-19 may signal future problems. “I think this is a serious concern,” DeRisi said. “If this trend increases, I expect we will see MIS-C growth.”
For now, they aim to use their study as a model for understanding others autoimmune or inflammatory conditions that can be caused by viral infections, such as diabetes OR multiple sclerosis.
This article is for informational purposes only and is not intended to provide medical advice.
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