Virally mediated changes in cellular permeability.

Abstract

Conferences on membranes are now held as frequently as those on intermediary metabolism or proteins were some years ago; few discussions of membranes, however, deal with disease. And of those that do, the word “virus” hardly ever appears in the index (e.g., Trump and Arstila 1975; Bolis et al. 1976; Miller and Shamoo 1977; Andreoli et al. 1978). Yet it is obvious that viral diseases involve the surface membrane of cells: the initial interaction between viruses and susceptible cells is at the cell surface, membrane damage is a characteristic feature of infected cells (e.g., Thigpen 1971; Fenner et al. 1974), the interplay between infected cells and the immune system takes place at the cell surface, and the action of interferon in protecting against viral attack begins at the cell surface. The features of the cell surface that have been particularly studied to date (e.g., Poste and Nicholson 1977) are the nature of virus receptors (proteins and glycoproteins), the mechanism by which viruses enter cells (endocystosis or, in the case of certain enveloped viruses, virus-cell fusion), the appearance of viral antigens (proteins and glycoproteins) on the surface of infected cells, the mechanism of viral release, and the participation of surface-bound antigens in eliciting an immune (cell-mediated) response. What has been relatively less explored is the way in which the cytopathic effects of viruses come about. The aim of this chapter is to suggest that a change in cellular permeability is at the root of some of these effects and that such a change may underlie the pathological consequences, that is, the diseases, that result from viral infection in certain cases.