Alex Eben Meyer
Long Covid has mystified scientists and doctors alike. Characterized by pain, fatigue, and other debilitating symptoms that continue for months or years after contracting Covid-19, its root causes remain elusive.
The potential culprit may be hiding among the body’s defenses: the immune system, which kicks into high gear when a person is infected with a virus. “In most cases, it will mount a response that’s specific to the virus, and not mount a response against us,” said Keyla Sá, postdoctoral researcher at Yale School of Medicine. But it’s possible for the immune system to temporarily attack the person’s own organs. “For some people, that never goes away.”
Sá works with Akiko Iwasaki, Sterling Professor of Immunobiology at Yale School of Medicine, who has spent years investigating whether a rogue immune system might be to blame for long Covid. In a study recently published in Cell, they report early evidence that at least some of the telltale symptoms of long Covid could be driven by misdirected immune molecules called autoantibodies.
Antibodies are proteins produced by the immune system to identify foreign materials for destruction by immune cells. However, autoantibodies identify the body’s own molecules as targets, which can lead to autoimmune diseases such as rheumatoid arthritis and lupus. When Sá tested patients with long Covid, she found many of them had autoantibodies with a surprisingly wide-ranging set of targets. “I was shocked by how diverse it was,” she says. “But later I realized that long Covid is a diverse disease where patients have different symptoms.”
To test whether autoantibodies could cause these symptoms, she injected autoantibodies from long Covid patients into mice. Within days, many of the mice started demonstrating behavioral changes. They became more tired running on a treadmill. Mice who received autoantibodies from patients with chronic pain showed signs of pain.
When Sá saw this, she realized that autoantibodies may be one possible driver of pain and fatigue in long Covid, but she emphasized that it may not be the only factor, or relevant to all patients. She plans to continue investigating these autoantibodies to better understand how particular antibodies lead to specific symptoms. Aparna Nathan ’17
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