A Mount Sinai-led research team has demonstrated that autoimmunity, when the body’s immune system attacks its own tissues, is responsible for the often debilitating and disorienting symptoms of long-term COVID-19 infections in some people.
The research results are cell The May 28 announcement could lead to important new approaches to treating patients with long-term COVID-19 infection, including already validated treatments for autoimmune management and new ways to clinically identify which patients are most likely to benefit from these treatments.
Although it has long been known that the novel coronavirus involves a variety of phenotypes, rather than just one, it has now been verified that autoimmunity is a major contributor to the symptom burden. New understanding of the long-term physiology of COVID-19 will help identify a number of effective treatments for autoimmunity that could significantly improve symptoms for the millions of people living with this chronic disease. ”
Dr. David Putrino, Nash Family Director of the Cohen Center for Recovery from Complex Chronic Illness at Mount Sinai, and co-senior author of this study
Research shows that between 4 and 20 percent of people infected with COVID-19 continue to experience symptoms such as persistent fatigue, cognitive impairment, heart palpitations, and joint and muscle pain for months or even years. The mechanisms behind the prolonged duration of the disease are thought to include viral persistence, reactivation of previously dormant viruses such as herpesviruses, and immune dysregulation in which the immune system struggles to reset after an infection has subsided, leading to ongoing inflammation and other health problems.
In this new study, researchers sought to better understand the different subtypes of the novel coronavirus and the involvement of the immune system in triggering long-term physical symptoms. To achieve this goal, the researchers collected and purified antibodies from the blood of 87 participants infected with the new coronavirus and injected them into healthy mice. The results were amazing.
Additionally, that awareness may inform which treatments are most likely to reduce symptom burden. For example, intravenous immunoglobulin (IVIG) contains antibodies from a healthy human donor and is commonly used to treat autoimmune diseases such as lupus by strengthening or regulating the recipient’s immune system. FcRn inhibitors are other biological agents that may help patients with long-term COVID-19 infection by reducing the amount of antibodies. IVIG and FcRn inhibitors have already been prescribed to some patients with long-term COVID-19 infections, but the results have been inconsistent, with some patients responding very well and others not responding. That, in turn, has dampened industry enthusiasm for long-term coronavirus research.
Scientists studying new repurposed therapies for the long-lasting coronavirus also include CAR T-cell therapy, which has the potential to genetically modify a person’s T cells to recognize and target harmful cells that secrete autoantibodies, and plasmapheresis, which can easily remove those autoantibodies from the system, Putrino said.
“Previously, there was no way to predict who would benefit from treatments such as IVIG or FcRn inhibitors,” he says. “Our study shows that if you belong to a subgroup of long-term COVID-19 patients who have autoantibodies circulating in their body, this is a quantifiable sign that you may be a good candidate for these drugs.”
In addition to its clinical implications, Dr. Putrino believes his research issues an urgent public health warning regarding the donation of blood and blood products such as plasma. He explained: “In the UK, prolonged illness with COVID-19 precludes blood donation, but in the US these individuals are still allowed to donate blood. Given the risk to others from the plasma of individuals with prolonged illness with COVID-19, this country should consider fundamental changes to its donation policy that reflect this health threat and are designed to fully protect its people.”
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