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On the membrane cytopathology of mouse hepatitis virus infection as probed by a semi-permeable translation-inhibiting drug.

Previous studies of the membrane fusion process have permitted the characterization of membrane permeability changes concomitant with MHV-induced cytopathology. One indication of membrane permeability in MHV-infected cells is their sensitivity to translation inhibition by the normally impermeable amino-glycoside, hygromycin B (Macintyre, G., Wong, F. and Anderson, R. (1989) J. Gen. Virol. 70, 763-768). In the present study, we examine the hygromycin B sensitivity of acutely infected mouse fibroblast L-2 cell and macrophage cultures as well as persistently infected mouse fibroblast LM-K cell cultures. The results suggest that membrane permeability alterations (as indicated by hygromycin B sensitivity) are a common feature of these MHV infections. Hygromycin B "cured" persistently infected LM-K cells as indicated by the absence of detectable virus antigen by immunofluorescence and by the absence of infectious virus even after removal of the drug or co-cultivation with untreated L-2 cells. The results argue against the maintenance of MHV infection by a mechanism involving latently or non-cytolytically infected cells. We conclude therefore that at least one mechanism for MHV persistence depends on virus propagation by cytolytic infection of a small, dynamically changing, fraction of the total cells present in culture.

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