A Common Cold Might Set Some Up for Long COVID

A Common Cold Might Set Some Up for Long COVID

Editor’s note: Find the latest long COVID news and guidance in Medscape’s Long COVID Resource Center.

A lot about long COVID remains a mystery. The relative newness of the condition and the heterogeneity of symptoms and presentations has researchers searching for some definitive answers. Also, knowing more about how and why long COVID develops could help healthcare providers offer more effective treatments.

People with rheumatic disease and a history of a specific type of cold virus infection called OC43 are at elevated risk for developing long COVID, new research reveals.

Because antibodies remain in the blood, OC43 could also serve as a biomarker to predict people who are more likely to experience long COVID, also known as postacute sequelae of coronavirus disease 19.

“Patients with rheumatic disease may be predisposed to long COVID because of their dysregulated immune responses from their disease and/or its treatments,” said study co-author Zachary Wallace, MD, a rheumatologist and physician investigator at Massachusetts General Hospital in Boston. Autoimmunity, fibrosis, and other pathologic processes unique to people with rheumatic disease make them an ideal first population to evaluate.

The study findings, published September 6 in Science Translational Medicine, could also apply to a wider group of people. “The findings observed in patients with rheumatic disease could be unique to this population but may be shared among people without rheumatic disease who develop long COVID,” he added.

All in the Family

It’s all relative. Both OC43 and SARS-CoV-2 are in the betacoronavirus family of viruses. The immune system of a person with an OC43 common cold history might mistake a later COVID virus infection for OC43 again. So it launches a defense against OC43, which only partially protects against COVID, leaving the person more vulnerable to developing long COVID.

“Our findings suggest that an enriched response to OC43 may be associated with worse outcomes,” said study co-author Jeffrey A. Sparks, MD, of the Division of Rheumatology, Inflammation, and Immunity at Brigham and Women’s Hospital in Boston. This means that people whose immune systems attacks COVID as a completely new infection might fare better.

“A stronger immune response to SARS-CoV-2 is likely preferred. Such a response may clear the virus more effectively,” Sparks added, “which could be a potential pathway that differentiates those with and without long COVID.”

The connection between a history of the OC43 cold and later long COVID was unexpected. “We initially expected that immune response to SARS-CoV-2 would be the most important marker and did not necessarily expect immune response to different pathogens to be as important contributors,” Wallace said.

The investigators compared people with and without long COVID symptoms in two groups. A discovery cohort included 43 people with rheumatic disease and a validation cohort assessed an additional 48 people.

Developing a serum biomarker based on antibody levels would not be technically difficult. However, Wallace said the study first needs to be replicated in different populations and within the current COVID situation. It’s also unclear what level of OC43 antibodies would put an individual at higher risk.

Outside Perspectives

“It is a fascinating study. It provides us with a level of information that is needed for patients,” said Fernando Carnavali, MD, director of the Mount Sinai Center for Post-COVID Care on the Upper Westside of New York City and an associate professor of medicine at the Icahn School of Medicine.

For example, Carnavali added, it can show patients that we are investigating the mechanisms behind long COVID, which is a real condition. “Some people don’t believe they have long COVID and their families don’t believe it either.”

He cautioned giving patients false hope because of the relatively small number of participants in the study. It would also be difficult to generalize these results, he added, “This is one group of patients. But we have to start somewhere. And it may take some time — serious research does not happen overnight.”

“There has been a lot of interest in why some patients develop long COVID and others don’t. The work here informs us more about the mechanisms that might explain what is happening. I think that is exciting,” said Oladunni Adeyiga, MD, PhD, who works on a multidisciplinary team led by Nisha Viswanathan, MD, that treats people with long COVID.

“There have been so many hypotheses and many have not completely panned out,” said Adeyiga, who is also assistant clinic professor in the UCLA Department of Medicine, Division of Infectious Diseases, in Los Angeles.

“We are learning how to take care of patients with this condition, but we really want to know why this happens,” Adeyiga said. “Having that kind of information can inform more therapeutics in this realm.”

The study was independently supported. Wallace, Sparks, Carnavalli, and Adeyiga have disclosed no relevant financial relationships.

Damian McNamara is a staff journalist based in Miami. He covers a wide range of medical specialties, including infectious diseases, gastroenterology, and critical care. Follow Damian on Twitter: @MedReporter. For more news, follow Medscape on Facebook, X (formerly Twitter), Instagram, and YouTube.

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