Prior infection with a common cold coronavirus may predispose some people to establish Long COVID
The findings recognize a potential marker that could help determine people at high risk of establishing Long COVID.
In a mission to debunk the origins and reasons for “Long COVID” or PASC, recent research indicate an unforeseen connection: the common cold infection, OC43.
A study recommends that “Long COVID” might be connected to immune inscribing, where past infection direct exposures influence actions to new infections. People with PASC showed weakened reactions to SARS-CoV-2 however stronger reactions to another coronavirus, OC43. This insight may direct future treatment and danger assessment.
While a number of risk factors for PASC have actually been proposed, we still dont understand what causes it or why some people get it and others dont. To further complicate matters, PASC may have different causes in various individuals.
Immune Responses and Long COVID.
Some individuals with PASC have changes in particular immune actions, suggesting an immune system for PASC. PASC is especially typical amongst individuals with systemic autoimmune rheumatic illness. These are chronic diseases, such as lupus, where the body immune system incorrectly targets the bodys own tissues to trigger swelling. As much as 45% of those with these rheumatic diseases who are infected with SARS-CoV-2 establish PASC.
Individuals with PASC showed weakened reactions to SARS-CoV-2 however stronger responses to another coronavirus, OC43. Some individuals with PASC have changes in specific immune actions, recommending an immune system for PASC. The group found that participants with PASC had much weaker antibody actions to SARS-CoV-2 than those without PASC. The more powerful the reaction to OC43 in people with PASC, the weaker their response to SARS-CoV-2. More research will be required to determine if and how this weak immune reaction might lead to PASC.
Research Findings and Antibody Responses
An NIH-funded research team– led by Drs. Zachary Wallace at Massachusetts General Hospital (MGH), Jeffrey Sparks at Brigham and Womens Hospital, and Galit Alter at MGH, MIT, and Harvard– analyzed antibody reactions in individuals with rheumatic diseases who had actually had COVID-19. They compared the responses of those who established PASC with those who didnt.
The group discovered that participants with PASC had much weaker antibody responses to SARS-CoV-2 than those without PASC. The more powerful the response to OC43 in individuals with PASC, the weaker their reaction to SARS-CoV-2.
Immune Imprinting and Its Implications
The findings suggest that PASC may emerge from a phenomenon understood as immune inscribing. This describes how a persons history of previous infections can impact their immune response to brand-new infections. In this case, when an individual who was formerly exposed to OC43 is contaminated with SARS-CoV-2, their body immune system reacts partially by utilizing antibodies developed throughout OC43 infection that also acknowledge SARS-CoV-2. This “recall” action to OC43 leads to an inefficient overall response to SARS-CoV-2. If and how this weak immune action may lead to PASC, further research study will be required to determine.
” When it pertains to viruses, first direct exposure can form long-lasting resistance,” Alter explains. “We understand that, in the setting of influenza, previous direct exposure to a viral strain can influence an individuals immune response to subsequent stress. This concept may be at play for coronaviruses, too, and may influence danger of Long COVID, particularly among people with rheumatic illness.”
The results may help discuss why PASC establishes, in at least some cases. They suggest a marker that could assist recognize people at high threat of establishing PASC for enrollment in more targeted clinical trials.
Recommendation: “Humoral immunity to an endemic coronavirus is associated with postacute sequelae of COVID-19 in people with rheumatic illness” by Jonathan D. Herman, Caroline Atyeo, Yonatan Zur, Claire E. Cook, Naomi J. Patel, Kathleen M. Vanni, Emily N. Kowalski, Grace Qian, Shruthi Srivatsan, Nancy A. Shadick, Deepak A. Rao, Benjamin Kellman, Colin J. Mann, Douglas Lauffenburger, Zachary S. Wallace, Jeffrey A. Sparks and Galit Alter, 6 September 2023, Science Translational Medicine.DOI: 10.1126/ scitranslmed.adf6598.
Financing: NIHs National Institute of Allergy and Infectious Diseases (NIAID), National Cancer Institute (NCI), National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), and National Center for Advancing Translational Sciences (NCATS); Nancy Zimmerman; Mark and Lisa Schwartz; Anonymous donor; Terry and Susan Ragon; Massachusetts General Hospital; Ragon Institute of MGH, MIT, and Harvard; Massachusetts Consortium on Pathogen Readiness; Bill and Melinda Gates Foundation; Global Health Vaccine Accelerator Platform; Musk Foundation; R. Bruce and Joan M. Mickey Research Scholar Fund; Rheumatoid Research Foundation; Doris Duke Charitable Foundation.
