P. Brown et al., THE DISTRIBUTION OF INFECTIVITY IN BLOOD COMPONENTS AND PLASMA DERIVATIVES IN EXPERIMENTAL-MODELS OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY, Transfusion, 38(9), 1998, pp. 810-816
BACKGROUND: The administration of blood components from donors who sub
sequently develop Creutzfeldt-Jakob disease has raised the issue of bl
ood as a possible vehicle for iatrogenic disease. STUDY DESIGN AND MET
HODS: We examined infectivity in blood components and Cohn plasma frac
tions in normal human blood that had been ''spiked'' with trypsinized
cells from a scrapie-infected hamster brain, and in blood of clinicall
y ill mice that had been inoculated with a mouse-adapted strain of hum
an transmissible spongiform encephalopathy. Infectivity was assayed by
intracerebral inoculation of the blood specimens into healthy animals
. RESULTS: Most of the infectivity in spiked human blood was associate
d with cellular blood components; the smaller amount present in plasma
, when fractionated, was found mainly in cryoprecipitate (the source o
f factor VIII) and fraction I+II+III (the source of fibrinogen and imm
unoglobulin); almost none was recovered in fraction IV (the source of
vitamin-K-dependent proteins) and fraction V (the source of albumin).
Mice infected with the human strain of spongiform encephalopathy had v
ery low levels of endogenous infectivity in buffy coat, plasma, cryopr
ecipitate, and fraction I+II+III, and no detectable infectivity in fra
ctions IV or V. CONCLUSION: Convergent results from exogenous spiking
and endogenous infectivity experiments, in which decreasing levels of
infectivity occurred in cellular blood components, plasma, and plasma
fractions, suggest a potential but, minimal risk of acquiring Creutzfe
ldt-Jakob disease from the administration of human plasma protein conc
entrates.