Infectious Disease

Data supports COVID-19 as an autoimmunity trigger in patients without pre-existing IMIDs

April 18, 2021

3 min read

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Calabrian LH. Advances in Understanding the Immunobiology of COVID-19 – Implications for Autoimmune Diseases and Autoinflammatory Diseases. Presented on: Interdisciplinary autoimmune summit. 15.-18. April 2021 (virtual meeting).

Disclosure:
Calabrese reports consulting fees from AbbVie, Amgen, Bristol Myers Squibb, Crescendo, Genentech, Gilead, GlaxoSmithKline, Janssen, Kiniksa, Eli Lilly, Pfizer, Sanofi / Regeneron and UCB, as well as fees from AbbVie, Bristol Myers Squibb, Crescendo, Genentech, Horizon , Sanofi and UCB.

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New data show that COVID-19 can trigger autoimmunity in patients without pre-existing immune-mediated inflammatory diseases, the consequences of which are still unknown, according to a spokesman for the Interdisciplinary Autoimmune Summit 2021.

“This raises several questions. Will this be able to flicker IMIDs? Will this cause new autoimmune diseases? Will It Contribute To Long COVID Syndrome? ” Leonard H. Calabrese, DO, Professor of Medicine at Cleveland Clinic Lerner College of Medicine and RJ Fasenmyer Chair of Clinical Immunology at Cleveland Clinic, said attendees at the virtual meeting.

“I think there is just so much going on here and we’re just putting our foot on the river,” Leonard H. Calabrese, DO, told attendees. “I’ll just leave you this thought: we are closer to the beginning than the end.” Source: Adobe Stock

“There is no doubt that viruses can induce autoimmunity,” he added. “We have seen patients with this infection before, as there are 40 million people on the planet who have had it – probably 50 million now. We see Guillain-Barré and immunocytopenias, but we still learn a lot. “

Calabrese highlighted four recent studies, three of which have not yet been published but are available in the medRxiv.org archive. He said they are detecting “significant autoantibodies” in patients who develop COVID-19. In one study, Nahid Bhadelia, MD, MA, from Boston University School of Medicine and colleagues reported data to support the induction of immune responses to self-epitopes during acute, severe COVID-19, with evidence of general B-cell hyperactivation.

Leonard Calabrese, DO

Leonard H. Calabrese

In another, Eric Y. Wang, of the Yale School of Medicine and colleagues concluded that their results show a pathological role for exoproteome-driven autoantibodies in COVID-19 with various effects on immune functionality and associations with clinical outcomes.

In the third study, which is still pending peer review, Sarah Esther Chang, from Stanford University School of Medicine and colleagues stated that SARS-CoV-2 triggers the development of emerging IgG autoantibodies in a significant proportion of patients hospitalized with COVID-19 that correlate positively with immune responses to SARS-CoV-. 2 proteins.

The group’s only published study appeared online in Nature in January. Inside, Alexis J. Combes, PhD, from the University of California, San Francisco, and colleagues reveal potential targets for immunotherapy in patients with severe COVID-19 to re-enable virus defenses.

“Most of these are not peer-reviewed … but they are four highly effective articles from the past few weeks that ultimately all agreed that patients with COVID-19 develop autoantibodies,” Calabrese said. “And that’s not just trivial [antinuclear antibodies] here and there – major autoantibodies. “

The most powerful of these studies, according to Calabrese, came from Chang and colleagues. This study was conducted by a senior author Paul J. Utz, MD, Stanford University School of Medicine had 147 patients from various centers – including Stanford and the University of Pennsylvania – all of whom were hospitalized with COVID-19.

According to the results, the researchers identified about 50% of the participants in autoantibodies.

“They used a very robust platform to look for autoantibodies, and the bottom line was that they found autoantibodies in half of those patients,” Calabrese said. “Some were temporary, but most were persistent, even well into recovery. And the final observation was that they appeared to be chasing with antiviral antibodies. “

According to Calabrese, the long-term effects of this and the aftermath of COVID-19 are generally still unknown. Data published in the Weekly Report on Morbidity and Mortality and in JAMA shows that 35% of patients with COVID-19 do not return to their normal health after 2-3 weeks, including 20% ​​of those with no previous chronic illness. In addition, 55% had three or more persistent symptoms 60 days after the onset of symptoms.

Of 4,182 cases of patients who defined themselves as “normal” before COVID-19, symptoms were reported by 13.3% after 4 weeks, by 4.5% after 8 weeks and by 2.3% after 12 weeks.

“Basically, this is a big problem, depending on how you define it,” said Calabrese. “A third. A quarter. Half. If we have tens of millions of people in this country who have had COVID-19, it means there are millions of people who have something that is syndromic there.”

He added, “I think there is just so much going on here and we are just putting our foot on the river. I just leave you this thought: we are closer to the beginning than the end. “

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Interdisciplinary autoimmune summit

Interdisciplinary autoimmune summit

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