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20 Interaction of Reovirus with Eukaryotic Host: Pathogenesis and Host Immune Response

Ann B. Georgi, Bernard N. Fields


To achieve productive infection, microbial pathogens must first overcome several host protective barriers. To accomplish this, pathogens have developed varied strategies to gain entry into host permissive tissue, replicate, spread within the host, and/or shed back into the environment while overcoming host defense mechanisms. For enteric viruses such as poliomyelitis, coxsackieviruses, and reovirus, entry through the alimentary tract requires that the virus particles be resistant to gut proteases and that they possess a mechanism for crossing the mucosal surface of the intestine to gain access to permissive tissue. Mammalian reoviruses have proven useful for the study of pathogenesis of enteric virus infection.

The molecular structure of reovirus (described by Nibert and Fields, this volume) has been well characterized. Briefly, the virion consists of a double icosahedral protein shell encapsulating a segmented double-stranded RNA genome. In recent years, much has been learned about specific gene products and their contributions to reovirus pathogenesis.

Three distinct serotypes of the mammalian reoviruses (designated types 1, 2, and 3) have been defined by hemagglutination-inhibition and neutralization analyses. Genetic reassortment of gene segments between serotypes occurs following mixed infection. The genetic contributions of each of the parental serotypes can be determined by differences in electrophoretic mobility of the genes on SDS gels (Ramig et al. 1977).

Phenotypic differences in pathways of spread and tissue tropism between the different reovirus serotypes and the property of genetic reassortment make reovirus a useful model for the study of mechanisms of molecular pathogenesis in enteric viruses.


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