Author index for volume 132

It has previously been shown that a strain of thymidine kinase (tk)-deficient mouse L-929 cells was unable to respond to murine β-interferon by induction of an anti-viral state and synthesis of double-stranded, RNA-dependent enzymes. Sensitivity to interferon can be restored by introducing into the cells a segment of Herpes simplex virus DNA containing the viral tk gene. It is shown here that not all Ltk(?) cell strains are resistant to interferon, suggesting that expression of a tk gene is not a prerequisite for response to interferon. Introduction of various genes into the resistant Ltk(?) strain, either alone or together with DNA containing the Herpes virus tk gene, leads to restoration of interferon sensitivity only when tk-containing DNA is inserted, showing that the activation of interferon responsiveness is not an artifact of the gene transfer, selection, and cloning procedures. The results imply that a component of the Herpes virus DNA introduced into the cells is able to activate interferon sensitivity.