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Parallel mechanisms in neuropathogenesis of enteric virus infections

Although an enormous amount of genetic, biochemical, and structural information has been gleaned from the various applications of molecular biology to the study of enteric viruses, knowledge of the fundamental biology of these viruses and the disease processes resulting from infection by them is still incomplete. Poliovirus, the first and most devastating enteric virus pathogen of humans to be recognized, has long served as the model for studying pathogenesis of enteric virus infections. During the 1940s and 1950s epidemics of poliomyelitis acutely focused attention on poliovirus. An extensive research effort culminated in the development of effective poliovirus vaccines, but as subsequent investigation subsided significant gaps were left in our understanding of the pathogenesis of this and other enteric viruses. The biochemical basis of virion stability, the mechanics of virus entry into a host, the determinants of virus spread causing generalized infection of the host, and particularly the means of penetration by viruses into the central nervous system (CNS) all remained unresolved issues. A number of observations on the biologic processes and genetic determinants of reovirus pathogenesis, as well as advances in research on other enteric viruses, have revived (and revised) some earlier observations and interpretations of data relevant to understanding these issues. In addition to providing a framework for further study, comparisons among this group of viruses suggest that there may be common features in the pathogenesis of enteric virus infections.