Abnormal forms of the herpes simplex virus immediate early polypeptide Vmw175 induce the cellular stress response.

Induction of the major stress response in chick embryo fibroblasts, which follows infection at 38.5 degrees C with the herpes simplex virus mutant tsK, was investigated. Synthesis of cellular stress proteins occurred only when the mutant form of an immediate early polypeptide, Vmw175, was overproduced. Infection with mutant in 1411, which has an amber (TAG) termination signal inserted between codons 83 and 84 of the gene encoding Vmw175 and therefore specifies a truncated portion of the polypeptide, failed to stimulate stress protein synthesis. The results suggested that the presence of abnormal forms of Vmw175 at high concentrations was the signal for induction of the stress response in tsK-infected cells.