This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maggioncalda, J Articles by Block, T M Search for Related Content PubMed PubMed Citation Articles by Maggioncalda, J Articles by Block, T M

 Previous Article  |  Next Article 

J Virol. 1994 December; 68(12): 7816-7824

Analysis of a herpes simplex virus type 1 LAT mutant with a deletion between the putative promoter and the 5' end of the 2.0-kilobase transcript.

Department of Microbiology and Immunology, Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107-6799.

ABSTRACT

A herpes simplex virus type 1 strain 17 mutant with a deletion between genomic nucleotides 118880 and 119250 was constructed and called 17 delta Sty. The deletion removes most of a putative secondary LAT promoter (called LAPII) as well as 370 of the first 449 nucleotides of the proposed 8.5-kb transcript believed to be the precursor of 2.0-kb LAT. 17 delta Sty was shown to produce major 2.0-kb LATs in tissue culture. Moreover, trigeminal nerves from latently infected mice contained an intact 1.45- to 2.0-kb LAT as well as the minor LATs which are recognized by probes specific for regions downstream of the 2.0-kb LAT. Finally, 17 delta Sty reactivated with normal kinetics from the trigeminal ganglia of latently infected mice in the explant cocultivation assay and egressed from tissue culture cells as efficiently as wild-type virus. These results clearly show that the region deleted in 17 delta Sty is dispensable for intact 2-kb LAT production, viral egress in tissue culture, and normal reactivation from latently infected neurons in mice.

This article has been cited by other articles:

• Bertke, A. S., Patel, A., Krause, P. R. (2007). Herpes Simplex Virus Latency-Associated Transcript Sequence Downstream of the Promoter Influences Type-Specific Reactivation and Viral Neurotropism. J. Virol. 81: 6605-6613 [Abstract] [Full Text]  
• Thompson, R. L., Sawtell, N. M. (2001). Herpes Simplex Virus Type 1 Latency-Associated Transcript Gene Promotes Neuronal Survival. J. Virol. 75: 6660-6675 [Abstract] [Full Text]  
• Perng, G.-C., Slanina, S. M., Ghiasi, H., Nesburn, A. B., Wechsler, S. L. (2001). The effect of latency-associated transcript on the herpes simplex virus type 1 latency-reactivation phenotype is mouse strain-dependent. J. Gen. Virol. 82: 1117-1122 [Abstract] [Full Text]  
• Jin, L., Schnitzlein, W. M., Scherba, G. (2000). Identification of the Pseudorabies Virus Promoter Required for Latency-Associated Transcript Gene Expression in the Natural Host. J. Virol. 74: 6333-6338 [Abstract] [Full Text]  
• Su, Y.-H., Meegalla, R. L., Chowhan, R., Cubitt, C., Oakes, J. E., Lausch, R. N., Fraser, N. W., Block, T. M. (1999). Human Corneal Cells and Other Fibroblasts Can Stimulate the Appearance of Herpes Simplex Virus from Quiescently Infected PC12 Cells. J. Virol. 73: 4171-4180 [Abstract] [Full Text]  
• Loutsch, J. M., Perng, G.-C., Hill, J. M., Zheng, X., Marquart, M. E., Block, T. M., Ghiasi, H., Nesburn, A. B., Wechsler, S. L. (1999). Identical 371-Base-Pair Deletion Mutations in the LAT Genes of Herpes Simplex Virus Type 1 McKrae and 17syn+ Result in Different In Vivo Reactivation Phenotypes. J. Virol. 73: 767-771 [Abstract] [Full Text]