Effect of Interferon on the Replication of Sendai Virus

Abstract

SUMMARYThe incorporation of [aH]uridine into the four species of RNA specified by Sendai virus in monolayers of chick embryo fibroblasts was inhibited to an equal degree by addition of purified chick interferon to cultures before infection with virus. The inhibition of RNA synthesis was dose-dependent. Similarly, [3H]uridine incorporation into RNA of virus nucleocapsid and polyribosomes was completely inhibited by pretreatment with interferon. When interferon was added 2 hr after infection, there were only small effects on the synthesis of total virus-specific RNA and significantly gr-ater reduction was observed in [SH]uridine incorporation into the RNA of nucleocapsid and polyribosomes. Although Sendal infection does not interfere with host-cell protein or RNA synthesis, interferon added 6 hr or later after infection did not affect any Sendai replicative functions.

Reproduction of Paramyxoviruses

“…The interference is specific for the homologous virus, and does not appear to require the production of interferon, although defective virions may induce interferon under certain conditions. With Sendai virus, defective virions does not induce interferon, and inhibition of standard virus by the defective virus is characterized by a greater inhibition of 50 S RNA than of 18 S , whereas interferon causes inhibition of all Sendai virus-induced species of RNA (Richman et at., 1970). Furthermore, the limitation of the interference to the homologous virus and the sensitivity to UV irradiation of the defective virions also argue against a role of interferon.…”