Abstract
Vesicular stomatitis virus was found to inhibit RNA synthesis in Krebs-2 carcinoma cells, even if replication of the virus was prevented by prior ultraviolet irradiation or by puromycin. Defective virus in undiluted passage stocks of low infectivity also retained the property of inhibiting cellular RNA synthesis. The rate and extent of this effect were dependent on multiplicity of infection. These experiments favor the hypothesis that a preformed toxic component of the virion is responsible for inhibition of cellular RNA synthesis, but they do not rule out the possibility of an inhibitory protein newly synthesized on an intact cistron of the infecting viral genome.