The α or immediate early mRNA of herpes simplex virus strain HSV-2(G) had a half-life of about 15 min if made in the absence of viral protein synthesis but was relatively stable if viral protein synthesis occurred, either freely or restricted by the presence of the proline analogue azetidine. In contrast, the α mRNA of other strains of the virus is stable, even in the absence of protein synthesis. Studies with recombinant viruses showed that the region of the viral DNA between 0.58 and 0.65 map units [which includes the gene (vhs, UL41) that controls virion-mediated shutoff of host protein synthesis] is important in determining the survival of α mRNA. In mixed infection experiments HSV-2(G) inhibited α as well as host protein synthesis but the shutoff activity appeared to be short-lived. Within 3 h after infection, as a result of protein synthesis, cells became completely resistant to shutoff by superinfecting virus.


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