Previous encounters of endemic coronaviruses connected to a COVID

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People who develop long-term COVID would likely react more strongly to a virus other than SARS-CoV-2 they found in the afterlife than to SARS-CoV-2, according to a study by researchers at Harvard Medical School.

Long COVID, also known as post-acute sequelae of COVID-19 (PASC), causes various symptoms that persist for at least four weeks after initial SARS-CoV-2 infection, they write on the medRxiv preprint server. Four authors explained their studies on the conceivable mechanisms of prolonged COVID in an interview.

“Immunity to non-endemic COVID coronaviruses would possibly play a role in PASC progression,” said co-director Jonathan D. Herman, MD, PhD. “There’s still a lot we want to understand, but it’s surprising that strengthening immune responses to the OC43 coronavirus has been uniquely enriched in other people with PASC. “

“In the study, other people with PASC preferentially generated stronger responses to cold-causing coronaviruses that were encountered in the past,” said co-director Galit Alter, PhD.

“Instead of generating strong immunity against SARS-CoV-2, they strengthened a reaction to another coronavirus, which could make their reaction less effective at eliminating SARS-CoV-2. Surprisingly, most Americans were vaccinated, and still maintained an unusual antibody reaction, indicating new avenues of healing for treating PASC,” Alter said.

One-fifth of COVID-19 patients progress to prolonged COVID, but it is well understood which patients expand PASC and why, the authors write.

“Antibodies are resistant biomarkers that have been used for decades to diagnose disease. However, antibodies also provide a solid source of data on past infections. The use of antibody profiles, here, highlighted the presence of incomplete antibody responses to SARS-CoV-2 in other people with PASC,” Alter said.

The researchers reviewed patients’ medical records at Mass General Brigham Health System in Boston, and added rheumatologist referrals from participants diagnosed with COVID-19 outside the MGB system, starting March 1, 2020.

They targeted patients with systemic autoimmune rheumatic diseases (SARS) because their tendency to inflammation and autoantibody production can make them more PASC and enriched with express inflammatory endotypes.

All 43 participants had COVID-19 without hospitalization and SARD. Patients treated for fibromyalgia, osteoarthritis, mechanical back pain, gout or pseudogout without SARD were excluded from the study.

Overall, 79% of participants were women, 35% had rheumatoid arthritis, 19% had psoriatic arthritis, and 95% had obtained a COVID-19 vaccine.

The researchers used formula serology to perform a complete SARS-CoV-2 antibody profile and a panel of endemic pathogens or regimen vaccine antigens.

Overall, 17 patients developed PASC and 26 did not, and in those with PASC, they found a distinct humoral immune response. PASC patients:

harbored fewer and weaker antibodies against SARS-CoV-2;

showed an expanded and more inflamed antibody reaction opposed to the endemic coronavirus OC43; and

generated more avid IgM responses and developed extensive inflammatory Fc receptor binding responses expressed in OC43 S2, which were linked to cross-reactivity between SARS-CoV-2 and common coronaviruses.

“The strengths of the study come with the detailed phenotypes of post-COVID-19 cases, specifically to classify the presence or absence of PASC, as well as the intensity and breadth of the antibody profile. This allowed us to identify a humoral immune signature of PASC,” said co-director Jeffrey A. Sparks, MD, MMSc.

“However, the study was limited to investigating other types of PASC, such as fatigue or lung symptoms, which could have biological differences. In addition, all patients in the study had pre-existing rheumatic disease,” he acknowledged.

“A significant portion of COVID-19 patients will expand PASC, which can have a very large impact on fitness and quality of life,” said co-senior author Zachary S. Wallace, MD, MS. of COVID-19 in many patients with rheumatic diseases, it is vital to perceive the etiology of PASC in this vulnerable population, to allow advances in diagnosis and long-term cure. “

Davey Smith, MD, a professor of medicine and leader of infectious diseases and global public fitness at the University of California, San Diego, La Jolla, who was not involved in the study, called the findings attractive, though the effects likely wouldn’t pass without delaying patient care.

“There would possibly be a link between a past infection with the non-SARS-CoV-2 coronavirus and PASC,” he added. “Perhaps by understanding why other people get and don’t get PASC, we can expand remedies for the disease. “.

“This document is a preprint and will have to go through peer review,” Smith said. “There are many elements that need to be analyzed. For example, there is no universally accepted definition of PASC, so how did that influence this?”study?”

Mark Cameron, PhD, an associate professor in the Department of Population and Quantitative Health Sciences at Case Western Reserve University, Cleveland, called this study a fake study of a fake group, although it is a preprint before peer review.

“In this initial study, scientists focused on other people who had rheumatic disease before contracting COVID-19, knowing that they are at increased risk for long-lasting headaches and are immunologically more similar when diagnosed with prolonged COVID – a single ‘endotype’ or organization. of patients with similar clinical symptoms and history. “He noticed.

“The memory of our immune system can’t fight well a new virus that looks too much like a virus you’ve seen before. This useless immune reaction can create various problems, adding to the poor recoveries we see in other people with prolonged COVID,” he said. .

“OC43 probably made the impression in the nineteenth century and probably caused a pandemic of severe respiratory illness between 1889 and 1890, which in the past was thought to be influenza,” Cameron recalled. “OC43 still presents itself as an endemic coronavirus, causing mild to moderate upper respiratory tract infections. “

Immunity to COVID-19 is complex, and a previous SARS-CoV-2 infection does not guarantee that we may not possibly contract COVID-19 again, especially as new variants emerge, added Cameron, who was also not involved in the study.

“This study may help us better understand the risks and conceivable mechanisms related to COVID-19 and prolonged COVID versus past coronavirus infections,” he said. “It can also help long-term consultants cure and COVID-19 vaccines. “

The authors plan a similar investigation.

The studio won a grant and an anonymous donation. Alter, Sparks and Wallace report financial relationships with the pharmaceutical industry. All other authors, as well as Davey and Cameron, report that there is no conflict of interest with the study. All experts commented on the email.

This story appeared in MDedge. com, which is part of Medscape’s professional network.

Credits:

Main image: Dreamstime

Image 1: Brigham and Women’s Hospital

Image 2: Brigham Mass General

Image 3: Brigham and Women’s Hospital

Image 4: Brigham and Women’s Hospital

Figure 5: University of California, San Diego Health

Image 6: Case Western University

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