title: An immunohistochemical study of the distribution of the measles virus receptors, CD46 and SLAM, in normal human tissues and subacute sclerosing panencephalitis.
abstract: We have compared the expression of the known measles virus (MV) receptors, membrane cofactor protein (CD46) and the signaling lymphocyte-activation molecule (SLAM), using immunohistochemistry, in a range of normal peripheral tissues (known to be infected by MV) as well as in normal and subacute sclerosing panencephalitis (SSPE) brain. To increase our understanding of how these receptors could be utilized by wild-type or vaccine strains in vivo, the results have been considered with regard to the known route of infection and systemic spread of MV. Strong staining for CD46 was observed in endothelial cells lining blood vessels and in epithelial cells and tissue macrophages in a wide range of peripheral tissues, as well as in Langerhans' and squamous cells in the skin. In lymphoid tissues and blood, subsets of cells were positive for SLAM, in comparison to CD46, which stained all nucleated cell types. Strong CD46 staining was observed on cerebral endothelium throughout the brain and also on ependymal cells lining the ventricles and choroid plexus. Comparatively weaker CD46 staining was observed on subsets of neurons and oligodendrocytes. In SSPE brain sections, the areas distant from lesion sites and negative for MV by immunocytochemistry showed the same distribution for CD46 as in normal brain. However, cells in lesions, positive for MV, were negative for CD46. Normal brain showed no staining for SLAM, and in SSPE brain only subsets of leukocytes in inflammatory infiltrates were positive. None of the cell types most commonly infected by MV show detectable expression of SLAM, whereas CD46 is much more widely expressed and could fulfill a receptor function for some wild-type strains. In the case of wild-type stains, which are unable to use CD46, a further as yet unknown receptor(s) would be necessary to fully explain the pathology of MV infection.
authors.affiliation: Neuropathology Laboratory, Royal Victoria Hospital, Queen's University Belfast, Northern Ireland. s.mcquaid@qub.ac.uk
authors.forename: Stephen
authors.initials: S
authors.lastname: McQuaid
authors.forename: Sara Louise
authors.initials: SL
authors.lastname: Cosby
mesh_terms: D015703:Antigens, CD / Q000378:metabolism*; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000821:virology; D006023:Glycoproteins / Q000378:metabolism*; D006801:Humans; D007124:Immunoenzyme Techniques; D007136:Immunoglobulins / Q000378:metabolism*; D008457:Measles / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins / Q000378:metabolism*; D011956:Receptors, Cell Surface; D011991:Receptors, Virus / Q000378:metabolism*; D000071177:Signaling Lymphocytic Activation Molecule Family Member 1; D013344:Subacute Sclerosing Panencephalitis / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D014018:Tissue Distribution
chemical_list: D015703:Antigens, CD; C497857:CD46 protein, human; D006023:Glycoproteins; D007136:Immunoglobulins; D051916:Membrane Cofactor Protein; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D011991:Receptors, Virus; D000071177:Signaling Lymphocytic Activation Molecule Family Member 1