Persistent Infection of L Cells with Vesicular Stomatitis Virus: Evolution of Virus Populations

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A previous report (Youngner et al., J. Virol. 19:90-101, 1976) documented that noncytocidal persistent infection can be established with wild-type vesicular stomatitis virus (VSV) in mouse L cells at 37°C and that a rapid selection of RNA−, group I temperature-sensitive (ts) mutants consistently occurs in this system. To assess the selective advantage of the RNA−ts phenotype, evolution of the virus population was studied in persistent infections initiated in L cells by use of VSV ts 0 23 and ts 0 45, RNA+ mutants belonging to complementation groups III and V. In L cells persistently infected with ts 0 23, the ts RNA+ virus population was replaced gradually by viruses which had a ts RNA− phenotype. VSV ts 0 45 (V) has another marker in addition to reduced virus yield at 39.5°C: a defective protein (G) which renders virion infectivity heat labile at 50°C. Persistent infections initiated with this virus (ts, heat labile, RNA+) evolved into a virus population which was ts, heat resistant, and RNA−. These findings suggest that the ts phenotype itself is not sufficient to stabilize the VSV population in persistently infected L cells and also indicate that the ts RNA− phenotype may have a unique selective advantage in this system. In addition to the selection of ts RNA− mutants, other mechanisms which also might operate in the maintenance of persistent VSV infections of L cells were explored. Whereas defective-interfering particles did not seem to mediate the carrier state, evidence was obtained that interferon may play a role in the regulation of persistent infections of L cells with VSV.

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