The present consensus is that the most likely route of infection of bovine spongiform encephalopathy (BSE) and new-variant Creutzfeldt-Jakob disease (vCJD) has been through the food chain-eating products contaminated with abnormal prion protein. The infectious prion then replicates in lymph tissues before moving through the nerves to the spinal cord or brain stem. Thus, anything that could impair replication of abnormal prions in the lymph nodes would delay the onset of clinical signs of this type of disease. Two papers in the April issue of Nature Medicine (Vol. 7, No. 4, 01 Apr 2001) report on a way that this could be achieved.
Neil Mabbott and colleagues at the Neuropathogenesis Unit in Edinburgh, Scotland, and Adriano Aguzzi's team at University of Zurich have discovered that depleting components of one part of the immune system called the complement system significantly delays the onset of disease symptoms in mice injected with scrapie.
The scientists treated mice with cobra venom factor (CVF), which is known to deplete levels of a complement molecule called C3 for five days. They then injected mice either intraperitoneally (i.p.) or intracerebrally with the infectious scrapie agent. For mice that had been infected i.p., the researchers discovered that those treated with CVF took longer to develop clinical symptoms of the disease than non-treated animals and that the early accumulation of abnormal prions in the spleen was reduced. The course of disease progression was the same in all animals that were infected by durect injection into the brain.
Franco Cardone and Maurizio Pocchiari from the Istituto Superiore di Sante in Italy discuss the experiments in an accompanying News & Views article.
Dr. Neil A. Mabbott
Institute for Animal Health,
Tel: + 11 44 131 667 5204
Fax: + 11 44 131 668 3872
Dr. Maurizio Pocchiari
Laboratory Superiore di Sanita
(C) Nature Medicine press release.
Message posted by: Trevor M. D'Souza