The relatively cell impermeable
hygromycin B was found to inhibit viral but not cellular
protein synthesis when added to cultures of murine hepatitis virus (MHV)-infected or mock-infected mouse L-2 fibroblasts. Membrane permeability, as judged by influx of
sodium ions, has previously been demonstrated to be an MHV E2
glycoprotein-mediated, cytopathic effect of MHV
infection in L-2 cells. It is therefore likely that the selective effect of
hygromycin B on
viral protein synthesis is a reflection of an increased
drug penetration into virus-infected cells. Using
hygromycin B as a marker for MHV-induced cell membrane cytopathology, the effects of
drug treatment on a persistent MHV
infection in mouse LM-K fibroblasts were investigated. MHV persistence in LM-K cells, which normally involves a steady state
infection of 0.1 to 1% of the cells in culture, was found to be cured by
hygromycin B treatment, as measured by the elimination of infectious virus from the supernatant medium.
Hygromycin B also resulted in the eradication of MHV-specific
RNA from LM-K cells, arguing against the presence of a non-cytopathically or latently infected subpopulation of cells.