Immune system may attack nervous system in some Long COVID patients
June 17, 2026
Immune system may attack nervous system in some Long COVID patients
At a Glance
- Researchers linked antibodies that attack the body’s nervous system to some neurological symptoms of Long COVID.
- The results may point to possible treatments for some people with Long COVID.
Some people infected with the virus that causes COVID-19 have symptoms that don’t go away after the infection does. This condition is called Long COVID. Manifestations of Long COVID vary from one person to another. Some people may experience neurologic symptoms such as headaches, fatigue, and difficulty thinking or concentrating.
Different biological processes may drive Long COVID symptoms in different patients. Scientists suspect one contributor may be an autoimmune reaction. In a healthy person, proteins called antibodies recognize and bind to specific microbes to help fight infections. In people with autoimmune disease, antibodies target the body’s own tissues instead. These are called autoantibodies. Researchers have found autoantibodies in some people with Long COVID.
A team of NIH-funded scientists, led by Drs. Akiko Iwasaki and Tamas L. Horvath of the Yale University School of Medicine and Dr. David Putrino of the Icahn School of Medicine at Mount Sinai, recently investigated the role of autoantibodies in neurological manifestations of Long COVID. The results of their research were published in Cell on May 28, 2026.
The scientists first studied antibodies from the blood of 147 people. Antibodies from patients with Long COVID and people who recovered from COVID reacted more often to human nervous system tissue than those of healthy people.
Long COVID patients whose autoantibodies targeted specific proteins or parts of the brain were more likely to have a set of similar symptoms. For example, people with autoantibodies targeting a brain area called the locus coeruleus were more likely to have lost their senses of taste and smell. They were also more likely to experience nausea and joint pain.
The team injected antibodies from the Long COVID patients into mice to see if the antibodies could cause Long COVID symptoms. They found that the test mice were more sensitive to pain if they received antibodies from Long COVID patients with chronic pain. Those mice also showed signs of nerve damage linked to chronic pain. Most of the mice that developed balance instability had received antibodies from patients with dizziness. The test mice also tired more quickly when placed on a moving treadmill.
“It is remarkable that mouse behavior mirrored some of the patients’ symptoms after their antibodies were transferred,” Iwasaki says.
The study suggests that autoantibodies play a key role in the neurological symptoms of some Long COVID patients. More research is needed to link specific autoantibodies to particular Long COVID symptoms. And the researchers note that autoantibodies may not be Long COVID’s only cause. Yet if these results are validated, this knowledge may guide treatment of a subset of Long COVID patients with therapies that target autoantibodies.
“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 says.
— by Brandon Levy
Related Links
- Immune and hormonal features of Long COVID
- Toward a deeper understanding of Long COVID
- Long COVID symptoms linked to inflammation
- Autoimmune response found in many with COVID-19
- Misdirected antibodies linked to severe COVID-19
- Your body’s disease defenses
- Understanding autoimmune diseases
- Long COVID basics (CDC)
References
A causal link between autoantibodies and neurological symptoms in long COVID. de Sá KSG, Silva J, Bayarri-Olmos R, Baker CA, Lu Z, Gipson W, Na D, Chen B, Wenxue L, Khosroabadi D, Brinda R, Constable RAR, Omene B, Colom Díaz PA, Kwon DI, Rodrigues G, Heidecke H, Schulze-Forster K, Gross A, Shneer T, Clarke A, Linnekin T, Brate A, Brown L, Buda H, Jatiani S, Moise L, Greene K, Bhagchandani S, Bhattacharjee B, Gehlhausen J, Wood J, Tabacof L, Scheibenbogen C, Liu Y, Guan L, Schneeberger Pane M, Putrino D, Horvath TL, Iwasaki A. Cell. 2026 May 28;189(11):3214-3235.e37. doi: 10.1016/j.cell.2026.04.042. PMID: 42208499.
Funding
NIH’s National Institute of Allergy and Infectious Diseases (NIAID); Howard Hughes Medical Institute; Else Kröner Fresenius Prize for Medical Research; RTW Foundation; Steve and Alexandra Cohen Foundation; Nash Family Foundation; Polybio Research Foundation; Yale Predoctoral Pharmacology Training Program; Pew Charitable Trusts.
