Mechanisms of vesicular stomatitis virus-induced cytopathic effects

Abstract

Abstract Vesiculuar stomatitis virus (VSV)-induced morphological alterations were studied in LLC-MK2 and BHK-21 cells. At a multiplicity of 200 plaque-forming units (PFU)/cell, VSV causes cell rounding in LLC-MK2 cells involving about 50% of the monolayer at 1 hr after infection (early cell rounding). Cycloheximide (300 μg/ml) does not prevent this but does inhibit further morphological changes (late cell rounding). The number of early rounded cells does not significantly increase when a multiplicity of 2900 PFU/cell is used in the presence of this drug. Early cell rounding is also not prevented in LLC-MK2 cells by either inhibitors of RNA synthesis (Proflavine, 6-azauridine) or uv- irradiation of the virus. BHK-21 cells infected at a multiplicity of 200 PFU/cell, in the presence of cycloheximide, show little cell rounding; however, there is a significant increase in the number of early rounded cells when infected at 2900 PFU/cell. LLC-MK2 cells infected with defective-interfering (DI) particles (2000 particles/cell) show the same degree of early rounding seen in cells infected with infectious virus at a comparable multiplicity. However, infection with DI particles does not cause late cell rounding. Defective-interfering particles used in these experiments exhibit no transcriptase activity either in vitro or in vivo and are unable to direct the synthesis of viral proteins in infected cells. These results indicate that an input viral structural component(s) is responsible for the early rounding of VSV-infected cells.