Virally mediated changes in cellular permeability.

syndrome platelets whose surface proteins were labelled with lz5I by the lactoperoxidase-catalysed procedure. A specific absence of radioactivity in the glycoprotein-Ib region of the gel may be observed; the other major membrane glycoproteins are normally labelled. Confirmation of the presence of glycoprotein IIIa was provided by Kunicki et al . (1978), who showed that BernardSoulier-syndrome platelets reacted normally with anti-(alloantigen P P ) antibody. Kunicki et al. (1978) observed, however, that Bernard-Soulier-syndrome platelets lacked another plateletspecific antigen marker, the receptor for quinineand quinidinedependent antibodies. Recently we have shown that this receptor activity was associated with a glycoprotein-Ib-enriched fraction purified by chromatography of Triton-X100-solubilized normal platelet membranes on wheat-germ-lectin affinity columns (A. T. Nurden, D. Dupuis, D. Pidard & T. J. Kunicki, unpublished work). That the Bernard-Soulier-syndrome platelets actually lacked glycoprotein Ib was further suggested by the studies of Hagen et al . (1980), who showed that a specific immunoprecipitate (band 13) was missing when Bernard-Souliersyndrome platelets were studied by crossed immunoelectrophoresis. Whereas band 13 was precipitated when normal human platelets were analysed against an antiserum prepared against isolated glycocalicin, no precipitate was observed with Bernard-Soulier-syndrome platelets. In conclusion, we have described evidence to show that two hereditary platelet disorders characterized by defects involving the two major pathways of platelet function in haemostasis, i.e. adhesion and aggregation, are associated with qualitatively different membrane glycoprotein deficiencies. These appear to be platelet-specific abnormalities; analysis of membranes isolated from erythrocytes of patients of both disorders revealed no glycoprotein defects. Elucidation of the mechanisms of platelet adhesion and aggregation is particularly important in view of the possible platelet involvement in the pathological processes leading to atherosclerosis and thrombosis. Studies such as we have described may offer clues to those membrane components which mediate the surface contact interactions vital to the specific functional activities of this remarkable cell.