Cellular sensitization in kuru, Jakob-Creutzfeldt disease and multiple sclerosis: with a note on the biohazards of slow infection work.
Following intramuscular injection of Kuru and Jakob-Creutzfeldt brain material into chimpanzees, circulating lymphocytes became sensitized to scrapie mouse brain (and spleen) to a greater degree than to normal tissue. This sensitization subsided after about a month, to be followed some 90 days later by a secondary peak attributed to establishment of changes in the nervous system. Special sensitization to scrapie material occurs in Kuru and Jakob-Creutzfeldt disease, but is not specific to them. The immunological evidence suggests that parenchymatous destruction may precede astroglial hypertrophy in these diseases. An early peak occurred in animals inoculated with multiple sclerosis brain and normal brain, but neither showed a delayed second peak. Thus there was no evidence of establishment of infection, even though all four animals were in intimate contact for over 200 days, and no evidence of the injection of MS material itself having established an infection. Biohazards in Kuru, Jakob-Creutzfeldt and MS work appear to be very low. The significance of the increased sensitilization to scrapie material in Kuru and Jakob-Creutzfeldt disease, especially in relation to normal ageing (where it also increases), is discussed.
D000818:Animals; D001921:Brain / Q000382:microbiology; D007562:Creutzfeldt-Jakob Syndrome / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D007729:Kuru / Q000276:immunology* / Q000635:transmission; D007757:Laboratory Infection / Q000453:epidemiology*; D008214:Lymphocytes / Q000276:immunology*; D008297:Male; D009103:Multiple Sclerosis / Q000276:immunology*; D002679:Pan troglodytes; D013997:Time Factors