Long COVID did not invent the post-acute phase of infection; it made it impossible to ignore. Acute infections are still often framed as time-limited events that end in recovery, deterioration or death, but this view fails to capture patients who remain biologically and clinically unwell after the acute infection has passed. The problem extends beyond SARS-CoV-2. Post-acute morbidity has been described after influenza, Epstein-Barr virus infection, Q fever, sepsis, and other infections, yet definitions, coding systems, and clinical pathways remain fragmented. We argue that post-acute infection should not be organized only by the initiating pathogen. Such pathogen-centric labels may be clinically tidy, but they risk producing heterogeneous cohorts, diluted biomarker signals, and disease-specific silos that obscure shared mechanisms of incomplete recovery. Instead, the field needs a second axis: the host-recovery state. Persistent inflammation, immune remodelling, loss of tolerance, antigenic stimulation, endothelial dysfunction, mitochondrial impairment, and tissue injury may represent overlapping immunometabolic failure modes across infections. Defining these states over time could help transform post-acute infection from a residual clinical label into a mechanism-informed framework for research, biomarkers, and care.
