Starting from the observation that the antiviral activity of cyclopentenone prostaglandins is associated with the synthesis of a 70K heat shock protein (HSP70), we have analysed the effect of short hyperthermic treatment (HT) on HSP70 induction and virus production in monkey epithelial cells during the replication of vesicular stomatitis virus (VSV). The heat shock response, as determined by HSP70 synthesis, appeared to be unaltered in VSV-infected cells in the first 4 h following virus infection, after which time it started to decline. No induction of HSP70 synthesis was observed when HT was applied 8 h after VSV infection. A 20 min HT at 45 degrees C was effective in suppressing VSV multiplication by more than 90% when applied at specific stages of the virus replication cycle. Synthesis of virus proteins was not affected by HT, indicating that the target for the treatment is a post-translational event. The HT-induced block of virus replication appeared to be associated with inhibition of VSV G protein maturation and HSP70 induction.
