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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 VSVts 0 23 andts 0 45, RNA+ mutants belonging to complementation groups III and V. In L cells persistently infected withts 0 23, thets RNA+ virus population was replaced gradually by viruses which had ats RNA− phenotype. VSVts 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 wasts , heat resistant, and RNA− . These findings suggest that thets phenotype itself is not sufficient to stabilize the VSV population in persistently infected L cells and also indicate that thets RNA− phenotype may have a unique selective advantage in this system. In addition to the selection ofts 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.

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