- Volume 52, Issue 2, 1981

Interferon induces an activity which strongly inhibits the growth of is-1, an interferon-response mutant of mengovirus. This activity is not expressed in protected cells infected with either is + (the wild-type parent) or vaccinia virus, or in cells infected with is-1 in the presence of actinomycin D. A failure of is-1 to shut off host RNA and/or protein synthesis could explain these observations. The present paper, however, shows that is-1 and is + are equally effective in suppressing host syntheses, and suggests that is + actively inhibits the interferon-mediated activity directed against is-1.

The pp60 src kinase activity of cells infected with temperature-conditional mutants of Rous sarcoma virus (RSV), which induce only a partial transformation, was compared to the pattern of transformation parameters induced by these mutants. The tsGI251-infected cells were thermosensitive for hexose transport, fibrinolysis, morphological alterations and pp60 src kinase activity, but cold-sensitive for loss of growth control. The tsGI253-infected cells were similar to tsGI251-infected cells except that they were only slightly cold-sensitive for loss of growth control and had a very low pp60 src kinase activity which was temperature-insensitive. Thus, the pp60 src kinase activity measured in vitro with IgG as a substrate did not correlate in a consistent way with any of the measured parameters of transformation.

The four known inhibitors of the bacterial DNA gyrase (nalidixic acid, oxolinic acid, novobiocin and coumermycin A) were investigated with respect to their effect on the growth of uninfected BHK cells and the yield of virus from herpes simplex virus type 1 (HSV-1)-infected BHK cells. High concentrations of nalidixic acid and oxolinic acid (about 10 mm) were needed for 50% inhibition of cellular and viral multiplication with less than fourfold preferential inhibition of virus over cell growth. Novobiocin and coumermycin were effective at lower molar concentrations and the amount needed for 50% inhibition was 10-fold higher for cell growth than for virus yield. At 5 × 10−4 m, novobiocin inhibited DNA synthesis in uninfected cells to approx. 20% of non-treated controls, while virus DNA in infected cells was almost completely inhibited (approx. 1% of controls). Residual cellular DNA synthesis in infected cells was rather insensitive (approx. 90% of controls) to this concentration of novobiocin.