The infectious prion then hijacks the body s machinery, reprogramming it into a willing executioner of prion replication. Since the disease s outbreak, it has been revealed that many common ailments including Alzheimer s disease and Parkinson s disease have similar properties.

The Prion Puzzle

Variant CJD was first described in 1996, following intensive surveillance activities undertaken by the UK National CJD Surveillance Unit (NCJDSU) in Edinburgh. This new form of prion disease had distinctive clinical and pathological features, and occurred in young patients within a single genetic subgroup.

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The host s body produces its own version of the prion protein, and it is difficult to create a high quality antibody against a body s own components. As a result, rather than trying to induce immunity, researchers must develop prefabricated anti prion antibodies that can be delivered directly to patients.

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My colleagues and I in NCJDSU argued that this new form of human prion disease was likely to be linked to exposure to the BSE agent, probably by eating BSE infected meat products. Later investigations have shown that the transmitting agent in variant CJD shares identical biological properties with BSE s agent, supporting a causal relationship.

The second case involved a known recipient of such cells transfused from another asymptomatic donor who subsequently died from variant CJD, whereas the recipient showed no evidence of neurological disease and died of unrelated causes. However, abnormal prion protein was detected in the recipient s lymphoid tissues, indicating transmission of infection from an asymptomatic individual.

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CJD belongs to the family of what are called prion diseases, a unique group of neurodegenerative diseases that can be transmitted. Although the precise nature of the disease s transmission remains uncertain, a key event in these disorders is the conversion of the prion protein s normal cells to an abnormal form that appears to be the major (if not the sole) component of the infection.

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