Aside from catching Covid itself, many other factors could increase the risk of someone developing long Covid – a chronic condition that develops after acute Covid infections and is characterized by a variety of symptoms, such as fatigue, breathing problems, or brain fog. Some of these risk factors include having asthma, type 2 diabetes, autoimmune conditions, or being female.
Now, a team of scientists led by Harvard University has found that patients with arthritis who developed long Covid showed evidence of an underwhelming antibody response to SARS-CoV-2, but a massive antibody response to OC43 – one of the several endemic coronaviruses that cause common colds.
The researchers tested the blood of 43 patients who had arthritis or a similar condition before the pandemic, and discovered that, when their immune systems were exposed to SARS-CoV-2, they responded with OC43 antibodies which, although similar, were less than ideal in fighting the novel coronavirus, leading to chronic inflammation and other long Covid symptoms.
According to Eric Topol, a professor of Molecular Medicine at Scripps Research, these new findings come in a “very interesting report that adds to the possible underpinnings of long Covid.” While previous research investigated the relationship between prior infections with the Epstein-Barr virus and other pathogens and long Covid risk factors, this is the first study to assess the role common cold may play in the development of this debilitating conditions.
However, the researchers warned that that are multiple categories of long Covid with, perhaps, different triggers for each type (aside from Covid itself). Thus, although prior infection with this common cold may play a role in arthritis patients with long Covid, it may or may not play a similar role in other categories of patients. Nonetheless, this discovery could serve as a way of identifying long Covid risk levels in arthritis patients and possibly find new ways of treating it.
A pre-print version of the study is published in medRxiv.
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