EFFECT OF HERPES-SIMPLEX VIRUS TYPE-1 U(L)41 GENE ON THE STABILITY OF MESSENGER-RNA FROM THE CELLULAR GENES - BETA-ACTIN, FIBRONECTIN, GLUCOSE TRANSPORTER-1, AND DOCKING PROTEIN, AND ON VIRUS INTRAPERITONEAL PATHOGENICITY TO NEWBORN MICE

Infection with HSV-1 is accompanied by the shut-off of cellular gene expression. The virion-associated function is encoded by the viral gene U(L)41. An HSV-1 mutant, vhs-1, which has a genomic deletion in the U(L)41 gene, is incapable of inducing the shut-off of cellular gene expression. The effect of HSV-1 infection on the shut-off of the cellular genes (or mRNA degradation) was studied specifically with the cellular genes for beta-actin, fibronectin, glucose transporter-1, and the docking protein. The level of these specific mRNAs was measured in cells infected with several HSV-1 strains and was compared to that of vhs-1- and mock-infected cells. It was possible to demonstrate a marked reduction in the level of the specific mRNA from these cellular genes in cells infected with several HSV-1 strains but not with the vhs-1 mutant. The pathogenicity of the HSV-1 vhs-I mutant to newborn mice was studied. It was found that the mutant is less pathogenic to newborn mice than its parental strain HSV-1 KOS.