Molecular genetics of herpes simplex virus. V. Characterization of a mutant defective in ability to form plaques at low temperatures and in a viral fraction which prevents accumulation of coreless capsids at nuclear pores late in infection

Abstract

In herpes simplex virus(HSV)-infected cells, coreless capsids accumulate at the nuclear pores soon after infection, but subsequently disappear, suggesting that, as in adenovirus-infected cells, the release of viral DNA from nucleocapsids takes place at the nuclear pores. A nonlethal mutant, HSV-1 (50B), produced by mutagenesis of HSV DNA fragments and selected for delayed production of plaques at 31.degree. C, accumulated coreless capsids at the nuclear pores late in infection in contrast to wild-type viruses. Recombinants selected for ability to produce plaques at 31.degree. C by marker rescue with digests of HSV-2 DNA and selected cloned fragments of HSV-1 DNA no longer accumulated empty capsids at nuclear pores late in infection. HSV apparently encodes a function which prevents accumulation of coreless capsids at nuclear pores, presumably by preventing uptake, unenvelopment and DNA release from progeny virus. The cold sensitivity of plaque formation and accumulation of coreless capsids might be related or comap in the S (short) component of the genome. [African green monkey kidney Vero, human laryngeal carcinoman HEp-2 and rabbit skin cells were used in this study.].