Laboratory analysis reveals that antibodies targeting SARS-CoV-2's nucleocapsid (N) protein exhibit cross-reactivity with multiple human cellular proteins across different tissue types. Using hyperimmune sera from three animal models, researchers identified molecular mimicry between viral N protein epitopes and host antigens in breast, kidney, immune, and intestinal cell lines. This cross-reactivity phenomenon provides a mechanistic explanation for the persistent autoimmune-like symptoms observed in long COVID patients. The nucleocapsid protein, while highly conserved and immunogenic, appears to trigger antibody responses that inadvertently target the body's own tissues. These findings carry significant implications for vaccine development strategies that incorporate N protein as an antigen. While natural infection generates robust anti-N antibody responses, the autoimmune potential suggests caution in designing N-based universal COVID vaccines. The research helps explain why some individuals experience prolonged inflammatory symptoms months after viral clearance, as circulating antibodies continue attacking molecular mimics in healthy tissue. For clinicians managing long COVID cases, this molecular mimicry mechanism suggests that immunosuppressive approaches rather than continued immune stimulation might prove more therapeutic. The work underscores the delicate balance between generating protective immunity and avoiding autoimmune complications in post-viral syndromes.