By G.H. Bourne, J.F. Danielli, K.W. Jeon (Eds.)
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C. Reoviruses . . . . . . . . . . . . . E. Retroviruses . . F. Coronaviruses. , . . . . . . . . . . . . . . . . . . . V. Virus-Receptor Interactions and Pathogenicity B. Role of Virus Attachment Proteins in Pathogenicity C. Induction of Cell-Specific Autoimmunity following Viral VI. Conclusion . . . . . . . . . . . . . . . References ................ 27 30 30 35 37 37 38 39 40 45 48 48 49 49 50 50 51 52 52 52 53 54 55 56 57 I. Definition of Viral Receptor Sites The definition of a receptor ultimately depends upon the structural and functional identification of a site that is specifically recognized by a ligand.
A variety of nomenclatures have been used to describe viral-receptor interactions, and depending on the context of the discussion several abbreviations will be used in this article. The protein by which the virus attaches to cells is the viral attachment protein (VAP). The “receptor” on the surface of the cell to which the virus binds is the cellular receptor site (CRS). Finally, it has been postulated that the CRS may be composed of multiple units and these units, which may bind a single VAP, are termed cellular receptor units (CRU) (Lonberg-Holm, 198 1).
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