Abstract
Transmissible spongiform encephalopathy agents (TSA) or prions induce neurodegenerative diseases in humans and animals. Their nature is still unknown, even if the main component of infectivity is identified as an abnormal isoform of a host-encoded protein, the prion protein (PrP). Today, no diagnostic test is available routinely for the detection of infected patients. TSA are resistant to most of the physical and chemical procedures that are efficient against other micro-organisms. Iatrogenic transmissions of TSA have been reported in the past: they always involved either brain derivatives or instruments that have been in contact with infected central nervous system. In an infected individual, infectivity is mostly detectable in brain. However, a persistent low-level viremia can be demonstrated in association with the white blood cells; infectivity is never found in plasma, serum or in red blood cells. Epidemiological data do not evidence any relationship between spongiform encephalopathies and blood transfusion. Therefore, in 1995, TSA transmission trough albumin is only a theoretical risk.
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