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Comparative analysis of normal prion protein expression on human, rodent, and ruminant blood cells by using a panel of prion antibodies
Author(s) -
Barclay G. Robin,
Houston E. Fiona,
Halliday Sue I.,
Farquhar Christine F.,
Turner Marc L.
Publication year - 2002
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.2002.00095.x
Subject(s) - infectivity , biology , transmissible spongiform encephalopathy , antibody , population , virology , flow cytometry , blood cell , immunology , bovine spongiform encephalopathy , scrapie , epitope , cell type , cell , human blood , prion protein , virus , medicine , genetics , pathology , physiology , disease , environmental health
BACKGROUND : It is not known whether variant CJD can be transmitted within the human population by blood transfusion. The expression of normal cellular prion protein (PrP C ) by different blood cell types may permit selective uptake and dissemination of infectivity. STUDY DESIGN AND METHODS : The normal distribution of PrP C on the major blood cell types of species known to be susceptible to natural or experimental transmissible spongiform encephalopathies was studied. Blood from healthy humans, mice, hamsters, cattle, and sheep was examined by flow cytometry by using a large panel of antibodies with different prion protein (PrP) epitope specificities to maximize the detection of PrP variants across species and cell type. RESULTS : PrP was detected on all major human blood cells types except eosinophils, but was not detected as ubiquitously or uniformly on major blood cell types of different animal species. CONCLUSION : Different animal species have unique patterns of expression of PrP C on blood cell types, with none equivalent to the human pattern. This needs to be considered when extrapolating from animal models of blood‐borne transmissible spongiform encephalopathy infectivity, particularly in regard to the risk assessment of potential variant CJD spread within the human population. The relationship between PrP distribution and infectivity distribution in blood needs further investigation.