Literature DB >> 11950898

An immunohistochemical study of the distribution of the measles virus receptors, CD46 and SLAM, in normal human tissues and subacute sclerosing panencephalitis.

Stephen McQuaid1, Sara Louise Cosby.   

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.

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Year:  2002        PMID: 11950898     DOI: 10.1038/labinvest.3780434

Source DB:  PubMed          Journal:  Lab Invest        ISSN: 0023-6837            Impact factor:   5.662


  33 in total

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4.  Weak cis and trans Interactions of the Hemagglutinin with Receptors Trigger Fusion Proteins of Neuropathogenic Measles Virus Isolates.

Authors:  Yuta Shirogane; Takao Hashiguchi; Yusuke Yanagi
Journal:  J Virol       Date:  2020-01-06       Impact factor: 5.103

Review 5.  Measles vaccination: Threat from related veterinary viruses and need for continued vaccination post measles eradication.

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Journal:  Hum Vaccin Immunother       Date:  2017-12-14       Impact factor: 3.452

6.  Cell-to-Cell Measles Virus Spread between Human Neurons Is Dependent on Hemagglutinin and Hyperfusogenic Fusion Protein.

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Journal:  J Virol       Date:  2018-02-26       Impact factor: 5.103

7.  Mutant fusion proteins with enhanced fusion activity promote measles virus spread in human neuronal cells and brains of suckling hamsters.

Authors:  Shumpei Watanabe; Yuta Shirogane; Satoshi O Suzuki; Satoshi Ikegame; Ritsuko Koga; Yusuke Yanagi
Journal:  J Virol       Date:  2012-12-19       Impact factor: 5.103

8.  Interleukin-13 displaying retargeted oncolytic measles virus strains have significant activity against gliomas with improved specificity.

Authors:  Cory Allen; Georgia Paraskevakou; Ianko Iankov; Caterina Giannini; Mark Schroeder; Jann Sarkaria; Mark Schroeder; Raj K Puri; Stephen J Russell; Evanthia Galanis
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9.  Measles virus interacts with human SLAM receptor on dendritic cells to cause immunosuppression.

Authors:  Bumsuk Hahm; Nathalie Arbour; Michael B A Oldstone
Journal:  Virology       Date:  2004-06-01       Impact factor: 3.616

10.  Changes in the receptorbinding haemagglutinin protein of wild-type morbilliviruses are not required for adaptation to Vero cells.

Authors:  Line Nielsen; Mads Klindt Andersen; Tove Dannemann Jensen; Merete Blixenkrone-Møller; Gert Bolt
Journal:  Virus Genes       Date:  2003-10       Impact factor: 2.332

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