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SUMMARY Evidence of recent infection with human parvovirus B19 (HPV) was found in two patients with early rheumatoid arthritis (RA) and in four patients with acute inflammatory arthritis (IA). Both of the patients with RA but only one of the four patients with IA carried RA associated haplotypes. No evidence of persistent infection with HPV was found, but evidence of past infection with HPV was significantly more common in patients with RA than in controls. The results confirm the arthritogenic potential of HPV and are consistent with the hypothesis that rheumatoid arthritis may develop in a genetically predisposed patient after an arthritogenic insult such as an HPV infection.

Rats can be passively protected against N. brasiliensis either with antiserum or with cells. Only some pools of antiserum (15 of 48 pools) and a few batches of cells (three of 11 batches) were protective.Protective activity was found in serum taken after one infection as frequently as after several infections and gave the same degree of protection. This suggests that second and subsequent infections do not stimulate an anamnestic increase in protective antibodies in the circulation.Serum and cells taken from the same rats were unrelated in their protective capacity; sometimes serum protected when the cells were ineffective and the reverse also occurred.Cells transferred from the spleen, peritoneal cavity or mesenteric lymph nodes were capable of initiating reagin formation, irrespective of their ability to protect against N. brasiliensis.When protection was achieved with transferred cells, the parasite life-cycle was shortened by only 1–2 days.We have found no evidence that a delayed mechanism of the homograft type is concerned in immunity to N. brasiliensis in the rat.We thank Miss W. D. Griffiths and Mr A. J. Edwards for their willing assistance. The statistical analysis was kindly done for us by Miss M. V. Mussett of the Statistics Department at our Institute.

Two-dimensional gel electrophoresis was used to analyse cerebrospinal fluid (CSF) from 75 suspect cases of bovine spongiform encephalopathy (BSE), 61 of which were confirmed by post mortem brain histopathology, and 38 normal cattle. CSF samples were also examined from cattle killed at periodic intervals through the incubation period following experimental challenge. Consistent changes were recorded in all CSF samples from the confirmed cases of natural BSE and also from cattle showing early signs of experimental disease. The changes consisted of an increased intensity of staining of apolipoprotein E and the presence of two protein spots, as yet unidentified, of molecular weights 35 and 36 kDa, both with a pI of 5.5. These changes were absent in the CSF samples from the normal cattle, from the clinically suspect cattle which were not confirmed as BSE and from the experimentally challenged cattle in the preclinical phase of infection.