June 1994
Volume 35, Issue 7
Free
Articles  |   June 1994
Similarities in regulation of the HSV-1 LAT promoter in corneal and neuronal cells.
Author Affiliations
  • G C Perng
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
  • J C Zwaagstra
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
  • H Ghiasi
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
  • R Kaiwar
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
  • D J Brown
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
  • A B Nesburn
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
  • S L Wechsler
    Ophthalmology Research Laboratories, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Investigative Ophthalmology & Visual Science June 1994, Vol.35, 2981-2989. doi:
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      G C Perng, J C Zwaagstra, H Ghiasi, R Kaiwar, D J Brown, A B Nesburn, S L Wechsler; Similarities in regulation of the HSV-1 LAT promoter in corneal and neuronal cells.. Invest. Ophthalmol. Vis. Sci. 1994;35(7):2981-2989.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To address the possibility of neuronal-like herpes simplex virus type 1 (HSV-1) latency in the cornea by determining if regulation of the HSV-1 LAT promoter in stromal keratocytes is similar to LAT promoter regulation in neurons. METHODS: Transient chloramphenicol acetyltransferase (CAT) assays were used to measure the relative promoter activity of various HSV-1 LAT promoter fragments in primary human corneal cells versus neuronal and nonneuronal cells. RESULTS: The authors found that the LAT promoter, whose location they previously mapped in neurons using transient CAT assays, functioned in stromal keratocytes using the same assay system and that two regions between -283 and -1932 nucleotides relative (upstream) to the start of LAT transcription slightly increased the LAT promoter activity in stromal keratocytes. They previously showed a similar increase in neuronal cells, and a large decrease in nonneuronal cells. In addition, they found that a neuronal specific enhancer region they previously defined between -162 and -283 nucleotides upstream of the start of LAT transcription also enhanced promoter activity in stromal keratocytes. Using gel-shift assays, they detected a nuclear factor specific to neurons and stromal keratocytes that binds to the LAT promoter and that may be a LAT regulatory factor. CONCLUSIONS: Recently, it has been suggested that the cornea might serve as an alternative site of latent herpes simplex virus type 1 (HSV-1) infection. However, this remains controversial. The authors' findings suggest that corneal and neuronal cells regulate the LAT promoter similarly and that this regulation differs from that seen in nonneuronal cells. Thus, the possibility of neuronal-like latency in the cornea remains plausible.

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