Researchers may have uncovered mechanisms underlying postacute sequelae of COVID-19 infection (also known as long COVID) in patients with systemic autoimmune rheumatic diseases, according to a study published by Herman et al in Science Translational Medicine. Researchers enrolled patients with systemic autoimmune rheumatic diseases who did or did not develop long COVID and used systems serology to conduct comprehensive antibody profiling against SARS–CoV-2, endemic pathogens, and routine vaccine antigens. Patients who developed long COVID demonstrated weaker Fc-gamma receptor–binding antibodies against the COVID-19 virus but harbored stronger Fc-gamma receptor–binding antibodies against the endemic coronavirus OC43. The new findings indicated that stronger receptor binding and presence of functional antibodies specific to the OC43 coronavirus may be linked to cross-reactivity across COVID-19 viruses and common coronaviruses and could point to previous coronavirus imprinting as a marker for the development of long COVID in patients with systemic autoimmune rheumatic diseases. The researchers hope to continue searching for biomarkers of long COVID—and may expand their analyses to patients without preexisting rheumatic diseases in order to determine whether their findings are applicable outside of the studied patient population.