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Journal of Virology, January 1999, p. 767-771, Vol. 73, No. 1
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

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

Jeannette M. Loutsch,1 Guey-Chuen Perng,2 James M. Hill,1 Xiaodong Zheng,1 Mary E. Marquart,1 Timothy M. Block,3 Homayon Ghiasi,2,4 Anthony B. Nesburn,2,4 and Steven L. Wechsler2,4,*

LSU Eye Center, Department of Ophthalmology, Microbiology and Immunology, and Department of Pharmacology, Louisiana State University Medical Center School of Medicine, New Orleans, Louisiana 70112-22341; Ophthalmology Research Laboratories, Cedars-Sinai Medical Center Burns and Allen Research Institute, Los Angeles, California 900482; Jefferson Center for Biomedical Research, Thomas Jefferson College, Doylestown, Pennsylvania 189013; and Department of Ophthalmology, UCLA School of Medicine, Los Angeles, California 900244

Received 25 August 1998/Accepted 13 October 1998

The herpes simplex virus type 1 (HSV-1) LAT gene is the only viral gene abundantly transcribed during latency. LAT null mutants created with strains McKrae and 17syn+ are impaired for both in vivo spontaneous and in vivo-induced reactivation. Thus, LAT is essential for efficient in vivo-induced and spontaneous reactivation. Different investigators have studied two LAT mutants containing a StyI-StyI region deletion corresponding to LAT nucleotides 76 to 447. One mutant, dLAT371 (parent strain, McKrae), had parental high frequencies of spontaneous reactivation. In vivo-induced reactivation was not examined. The other mutant, 17Delta Sty (parent strain, 17syn+), had parental frequencies of in vitro reactivation following cocultivation of explanted ganglia but reduced frequencies of in vivo-induced reactivation. Spontaneous reactivation frequency was not reported for 17Delta Sty. These combined results suggested the possibility that in vivo spontaneous reactivation and in vivo-induced reactivation may map to different regions within the LAT domain. We now report that dLAT371 has in vivo-induced reactivation frequencies of the parent and that 17Delta Sty has reduced frequencies of in vivo spontaneous reactivation. Thus, dLAT371 demonstrated the parental phenotype for both in vivo spontaneous and -induced reactivation while the apparently identical 17Delta Sty was impaired for both in vivo spontaneous and -induced reactivation. These results suggest that one or more differences between the genetic backgrounds of McKrae and 17syn+ result in different in vivo reactivation phenotypes of otherwise identical deletion mutations and that McKrae may have compensating sequences sufficient to overcome the loss of the StyI-StyI region of the LAT transcript.

* Corresponding author. Mailing address: Ophthalmology Research Laboratories, Cedars-Sinai Medical Center Burns and Allen Research Institute, Davis Bldg., Room 5072, 8700 Beverly Blvd., Los Angeles, CA 90048. Phone: (310) 855-6457 or (310) 855-6455. Fax: (310) 652-8411. E-mail: Wechsler{at}CSMC.EDU.

Journal of Virology, January 1999, p. 767-771, Vol. 73, No. 1
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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