The Induction of Interferon by Vesicular Stomatitis Virus in Mouse L Cells

Abstract

AbstractAlthough no detectable interferon was produced when L cells were infected with wild‐type VSV (VSV‐o), considerable amounts of interferon were produced when cells were infected with UV‐irradiated VSV‐o at a multiplicity equivalent to 10 PFU/cell. Treatment of VSV‐o with UV‐light resulted in the marked reduction of the RNA synthesizing capacity and cytotoxity of the virus, and the UV‐irradiated virus had neither infectivity nor interfering activity against homologous viruses. The amount of interferon induced by UV‐VSV‐o was markedly influenced by multiplicity of infection and incubation temperature. Less‐virulent temperature‐sensitive mutants (VSV‐mp and VSV‐sp) derived from L cells persistently infected with VSV induced interferon in L cells without treatment of the viruses with UV‐light, but these viruses could not induce interferon if the infected cells were incubated at nonpermissive temperature, or if cells were infected at multiplicities of more than 10 PFU/cell. On the other hand, it was shown that treatment of cells with cycloheximide (100 μg/ml) delayed the expression of cell damage caused by non‐irradiated VSV‐o and resulted in the production of interferon when cycloheximide was removed from the cultures. These results indicate that VSV has intrinsically interferon‐inducing capacity in L cells and can induce interferon if the induction is carried out under such condition that cell damage caused by VSV are suppressed or delayed. Furthermore, the effect of pretreatment of cells by interferon and undiluted passage of VSV‐o on interferon induction was discussed in relation to persistent infection.