Abstract

INTRODUCTION General The purpose of this chapter is to discuss the distribution of the poliovirus receptor (PVR) in human tissues with regard to its role in poliovirus (PV) pathogenesis; that is, in causing poliomyelitis. After the historical background of this problem is discussed, the identification of the PVR gene is summarized. A description of the present state of knowledge concerning the PVR protein(s) follows. A discussion of the current unresolved scientific issues closes the chapter. The PVR gene and its gene product(s) have turned out to be surprisingly complex; experimental results have often raised more questions than they answer. In the interest of precision, I use the abbreviation “PVR” when discussing issues relevant to the cloned reagent and the full phrase “PV receptor” when referring to the biological activity. Viruses can bring about tissue destruction, and therefore disease, in various ways: cytolysis, immune damage, toxic products, and cell transformation (Dulbecco and Ginsberg 1988). It is thought that PV kills neurons by direct cellular killing (Bodian 1959). Therefore, pathogenesis by virulent strains of PV is the direct effect of a characteristic, restricted range of cytopathic viral replication. The well-accepted premise of current molecular studies of viruses is that there are both virus-encoded and host-encoded determinants of virulence and, thus, disease. For both virus-encoded and host-encoded determinants of virulence, these specific molecules can contribute to viral life cycles in two distinct ways: by mediating viral host range or by mediating tissue tropism. The term “host-range determinant” refers to a characteristic that affects...

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