A Mount Sinai-Yale team has shown that transferring purified antibodies from 87 long COVID patients into healthy mice reliably induced pain behaviors, directly implicating autoantibodies in symptom generation. This is an observational antibody-transfer model, not an RCT, with modest sample size and no reported industry conflicts disclosed in the Cell publication. The work validates autoimmunity as a distinct phenotype amid viral persistence and latent-virus reactivation mechanisms previously outlined in larger cohort studies. What prior coverage missed is the convergence with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) literature, where similar IgG transfer experiments in the 2010s produced comparable fatigue and pain phenotypes, suggesting a shared post-viral autoimmune pathway rather than isolated SARS-CoV-2 effects. Synthesizing this with a 2023 Nature Reviews Immunology analysis of 1,200 post-acute sequalae cases and a 2022 Lancet Microbe observational study of EBV reactivation in 300 COVID survivors reveals a coherent pattern: molecular mimicry and bystander activation sustain autoreactive B-cell clones long after viral clearance. Clinically, this predicts differential response to FcRn inhibitors or IVIG, already used off-label in lupus; non-responders likely harbor dominant viral-persistence drivers instead. CAR-T and plasmapheresis warrant controlled trials stratified by autoantibody profiling to avoid the inconsistent outcomes seen in unstratified compassionate-use series.