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1 Medical Research Council Virology Unit, Church Street, Glasgow G11 5JR
and2 Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, U.K.
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.
Received 23 October 1989;
accepted 16 February 1990.
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