Abstract
Herpes simplex virus (HSV) particles contain a factor which can shut off host protein synthesis during the earliest stages of infection. The efficiency of shutoff varies between different strains of virus, type 2 strains being generally more active than type 1 strains. However, HSV-2 strain HG52 is deficient in host cell shutoff. We have investigated the basis of the different shutoff phenotypes of a strong shutoff strain (HSV-2 strain G), a weak shutoff virus (HSV-1 strain 17 syn+) and HG52 by comparative DNA sequence analysis of gene UL41, which encodes the virion-associated host shutoff factor. The results show that the UL41 genes of strains G and 17 are 86% homologous and that the lack of shutoff by HG52 is likely to be explained by a frameshift mutation within its UL41 coding sequence.