Post-acute infection syndrome

[1] The onset of symptoms may be delayed, often by decades in the case of post-polio syndrome, and their severity may fluctuate over time.

[1] The pathophysiology of most PAISs is poorly understood, but the overlap in symptoms despite disparate infectious triggers implies a possible shared pathology.

[1] Major hypotheses include persistence of the original pathogen or its remnants, autoimmunity, chronic inflammation, reactivation of other latent infections, microbiome dysbiosis, or damage to organs, which may include the lungs, brain, kidneys, heart, or blood vessels.

[1][3] In the absence of tests for most PAISes, diagnosis is usually based on the patient's history, symptoms, and eliminating other potential causes.

[1][3] Other known sequelae of infections include multisystem inflammatory syndrome in children (MIS-C), and subacute sclerosing panencephalitis (a deadly consequence of measles that can be delayed by years).

[4][5] Data on epidemiology is limited by the lack of large, rigorous studies; and rates vary by infection.

An Australian study of EBV, C. burnetii, and Ross River Virus found that 11% of participants met the criteria for ME/CFS at 6 months.

[1] While PAISs were described prior to the COVID-19 pandemic, the emergence of long COVID brought them increased attention.

Chart showing symptoms of long COVID
Microscope slide of cells infected with EBV
Cells infected with Epstein–Barr virus , one of the viruses implicated in PAISs
ME/CFS has many competing definitions.