L cells were treated with 100 reference units/ml of mouse interferon and then infected with a wild-type vesicular stomatitis virus (VSV) at a multiplicity of 10 to 60 p.f.u./cell. Prolonged infection of cultures ensued, lasting from 14 to at least 60 days. Less than 1% of the cells produced infectious virus, but more than 10% produced detectable levels of VSV antigens. No small virion RNA forms (< 42S) characteristic of defective interfering (DI) virus particles were detected. The virus produced appeared to be temperature sensitive. There was decreased plaquing efficiency at 37 or 39 °C compared to 32 °C and termination of the chronic infection due to c.p.e. within a few days after shift to 32 °C. The cultures resisted superinfection with wild-type VSV or with a heterologous virus, encephalomyocarditis (EMC) virus. Treatment of cultures with rabbit anti-mouse interferon globulin resulted in a marked increase in virus titres and termination of the chronic infection. Prolonged VSV infection in this system may be related both to the emergence of temperature-sensitive mutants and to endogenous interferon production rather than to cyclical generation of DI particles.


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