Prion diseases are categorized into three groups: sporadic, inherited, and acquired. Most slow virus infections-approximately 85%-are sporadic. The remaining 15% consist of hereditary forms (hereditary Creutzfeldt-Jakob disease [CJD], Gerstmann-Straussler-Scheinker disease, fatal familial insomnia) and acquired forms. Acquired forms may be transmitted iatrogenically (through human growth hormone therapy, dura mater grafts, or other neurosurgical procedures) or through cannibalism (kuru).
Slow virus infections are also known as prion diseases, after the presumed infectious agent, as well as transmissible spongiform encephalopathies (TSEs), after the histopathologic changes associated with these infections.
Prions are proteinaceous infectious particles (PrPs). The brain pathology of prion diseases consists of a vacuolar (spongiform) degeneration of the neuropil, cortical neurons, and subcortical gray matter with neuronal loss and gliosis. Early diagnosis is difficult, in part because prions do not have nucleic acids, making conventional nucleic acid-based viral detection systems ineffective. PrPs also elude detection by not producing a humoral immune response.
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