Abstract
Retroviruses are associated with a wide spectrum of diseases affecting vertebrate hosts, ranging from bony fish to mammals, and including humans. Genetic and interference studies have demonstrated the variety of receptors recognized by the different virus strains, although the extent to which these retroviral receptors determine the pathogenesis of any particular strain is still largely unknown. During the course of vertebrate evolution, retroviral genomes have on occasion become incorporated and maintained in the host germ line [1]. Such “endogenous” viruses must give some selective advantage to the host to be preserved in this way, and indeed endogenous viral proteins are frequently expressed. Such viruses, however, are often xeno-tropic [2]; that is, they cannot reinfect the cells of the species that harbor them but are infectious to foreign cells. It would appear that the host allows some viral expression but blocks the cell-to-cell spread of activated virus by receptor incompatibility. In some cases the host species does not express the relevant receptors; in others the receptors are blocked by an endogenous interference phenomenon [3,4]. The nature of most receptor molecules has not been elucidated; indeed, the only receptor that has been clearly identified is the CD4 antigen utilized by the human and simian immunodeficiency viruses (HIV and SIV respectively) [5].
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Sommerfelt, M.A., Weiss, R.A. (1989). Retrovirus Receptors and Cell Tropism. In: Notkins, A.L., Oldstone, M.B.A. (eds) Concepts in Viral Pathogenesis III. Springer, New York, NY. https://doi.org/10.1007/978-1-4613-8890-6_11
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DOI: https://doi.org/10.1007/978-1-4613-8890-6_11
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