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Journal of Virology, January 2000, p. 33-41, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Herpes Simplex Virus Type 1 Gene UL14: Phenotype of a Null Mutant and Identification of the Encoded Protein

Charles Cunningham,1,2 Andrew J. Davison,1,2,* Alasdair R. MacLean,2 Naomi S. Taus,3 and Joel D. Baines3

MRC Virology Unit1 and Division of Virology,2 Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G11 5JR, United Kingdom, and Department of Microbiology and Immunology, Cornell University, Ithaca, New York 148533

Received 6 July 1999/Accepted 20 September 1999

Herpes simplex virus type 1 (HSV-1) gene UL14 is located between divergently transcribed genes UL13 and UL15 and overlaps the promoters for both of these genes. UL14 also exhibits a substantial overlap of its coding region with that of UL13. It is one of the few HSV-1 genes for which a phenotype and protein product have not been described. Using mass spectrometric and immunological approaches, we demonstrated that the UL14 protein is a minor component of the virion tegument of 32 kDa which is expressed late in infection. In infected cells, the UL14 protein was detected in the nucleus at discrete sites within electron-dense nuclear bodies and in the cytoplasm initially in a diffuse distribution and then at discrete sites. Some of the UL14 protein was phosphorylated. A mutant with a 4-bp deletion in the central region of UL14 failed to produce the UL14 protein and generated small plaques. The mutant exhibited an extended growth cycle at low multiplicity of infection and appeared to be compromised in efficient transit of virus particles from the infected cell. In mice injected intracranially, the 50% lethal dose of the mutant was reduced more than 30,000-fold. Recovery of the mutant from the latently infected sacral ganglia of mice injected peripherally was significantly less than that of wild-type virus, suggesting a marked defect in the establishment of, or reactivation from, latent infection.

* Corresponding author. Mailing address: MRC Virology Unit, Church Street, Glasgow G11 5JR, United Kingdom. Phone: 44 141 330 6263. Fax: 44 141 337 2236. E-mail: a.davison{at}vir.gla.ac.uk.

Journal of Virology, January 2000, p. 33-41, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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