Cell reports. MedicineMar 25, 2026

Antibodies from long COVID patients cause symptoms when given to mice

Updated Jun 28, 2026

Abstract

Essence

IgG from long COVID patients induced persistent mechanical hypersensitivity in mice, supporting a possible autoantibody-driven component of long COVID.

Evidence

This translational preclinical transfer study injected pooled total IgG from biomarker-stratified long COVID patient subgroups into mice and found reproducible mechanical allodynia, including with IgG collected 2 years later from still-symptomatic patients.

Caveat

The main result is a mouse pain-like phenotype from pooled patient IgG, so it does not show that the same antibodies cause the full spectrum of long COVID symptoms in humans.

Simplified

SARS-CoV-2 infections have led to a surge in long COVID, a post-infectious syndrome in which autoantibodies are proposed to play a pathogenic role, analogous to fibromyalgia. Here, we test this hypothesis by transferring total IgG from long COVID patients into mice. We stratified patients into three subgroups using plasma levels of glial fibrillary acidic protein (GFAP), neurofilament light chain (NFL), and interferon-β, with subgroup-specific pathways supported by plasma proteomics. Transfer of pooled total IgG induces pronounced and persistent mechanical hypersensitivity. Notably, IgG collected 2 years later from the same long COVID patients who remained symptomatic reproduced mechanical allodynia in mice, demonstrating longitudinal stability of pathogenic activity. Proteome-wide autoantibody profiling identifies elevated, subgroup-linked autoreactivities that persist over time and are validated by independent assays. Together, these findings demonstrate that long COVID IgG can induce mechanical hypersensitivity in mice, support a causal role for autoantibodies in long COVID pathogenesis, and may establish a murine model for therapeutic development.