Researchers identified autoantibodies as a driver of long COVID symptoms in a subset of individuals, suggesting new treatment pathways.
RT’s Three Key Takeaways:
- Autoimmune Driver Identified: Research shows that the body’s immune system attacking its own tissues is responsible for the symptoms of long COVID in specific patient groups.
- Targeted Therapy Potential: The presence of circulating autoantibodies can serve as a clinical marker to identify patients who may benefit from treatments like intravenous immunoglobulin or FcRn inhibitors.
- Blood Donation Concerns: Study authors suggest that United States (US) blood donation policies should be reevaluated because of potential risks associated with plasma from individuals with long COVID.
A research team led by Mount Sinai has demonstrated that autoimmunity is responsible for the debilitating symptoms of long COVID in a subset of patients, according to a study published in Cell.
The findings could lead to new clinical approaches for identifying and treating patients using existing therapies for autoimmunity management. “We’ve known for some time that long COVID involves not just one but a variety of phenotypes, and now we have validated that autoimmunity is a major contributor to the symptom burden,” said David Putrino, PhD, nash family director of the cohen center for recovery from complex chronic illness at Mount Sinai and co-senior author of the study, in a news release.
Between 4% and 20% of people infected with COVID-19 experience symptoms such as persistent fatigue, cognitive impairment, heart palpitations, and joint and muscle pain for months or years. While mechanisms like viral persistence and immune dysregulation are known factors, this study focused on how the immune system triggers physical symptoms through autoantibodies.
Researchers purified antibodies from the blood of 87 participants with long COVID and infused them into healthy mice to observe the effects. The results validated that autoimmunity is a major contributor to the symptom burden in certain phenotypes of the disease.
The study suggests that patients with circulating autoantibodies may be candidates for biologic agents like intravenous immunoglobulin (IVIG) or FcRn inhibitors. IVIG contains antibodies from healthy donors used to regulate the immune system, while FcRn inhibitors help lower the amount of harmful antibodies. Other potential therapies being investigated include CAR-T cell therapy and plasmapheresis to remove autoantibodies from the system.
“Before we had no way of predicting who would benefit from therapies like IVIG or FcRn inhibitors,” said Putrino, nash family director of the cohen center for recovery from complex chronic illness at Mount Sinai and co-senior author of the study, in a news release. “Our study now shows that if you are in a subgroup of long COVID patients who have autoantibodies circulating in your body, this is a quantifiable sign that you may be a good candidate for these drugs.”
Putrino also raised concerns regarding blood and plasma donation policies in the US. Unlike the United Kingdom (UK), which excludes individuals with long COVID from donating blood, the US currently allows it. Putrino said the US should consider policy changes to protect the public from potential health threats posed by plasma from individuals with long COVID.
