Reactivation from quiescence does not coincide with a global induction of herpes simplex virus type 1 transactivators

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13 Scopus citations


Herpes simplex virus type 1 (HSV-1) reactivates from a small fraction of latently infected neurons in vivo and neuronally differentiated (ND), quiescently infected (QIF)-PC12 cells in vitro. This may be the result of reactivation initiating in only a few cells, or reactivation followed by premature termination of the productive virus life cycle in many or even a majority of cells. To examine the viral stress response, HSV-1 promoters of representative α, β, and γ class genes were examined in ND- and QIF-PC12 cells after treatments with agents known to induce reactivation. HSV-1 promoters displayed variable levels of basal gene expression in ND-PC12 cells ranging from 2 to 1,200 times the level of the control vector pGL3-Basic. Expression of the latency associated transcript (LAT) was greatest, with representatives of the α class exhibiting greater expression than the β and γ classes. The HSV-1 promoters examined did not respond dramatically to stress treatments. The viral gene response was also measured during the initiation of reactivation of a cryptic HSV-1 genome after forskolin treatment, under conditions that restricted DNA replication. During the first 24 h after stress induction the response was limited. By 48 h post-forskolin treatment, only modest increases occurred for ICP0, ICP4, and LAT transcripts, reaching levels of no greater than 2.2 times mock treated levels. In contrast, ICP27, ribonucleotide reductase (RR), and VP16 promoters did not respond. These findings indicate that reactivation from QIF-PC12 cells does not result in a global response of the specific HSV-1 genes tested, when assessed at the population level. These data support the hypothesis that stress-induced reactivation initiates in a minority of cells.

Original languageEnglish
Pages (from-to)163-167
Number of pages5
JournalVirus Genes
Issue number2
StatePublished - Oct 2006

Bibliographical note

Funding Information:
Acknowledgments We thank R. Thompson for plasmid pE-coE + K, M. Killen and T. Birkenhauer for providing technical assistance, and M. Steiner for helpful discussions. This research was supported by a grant from the National Institute of Dental Craniofacial Research, DE014142 (CSM).


  • Gene induction
  • Herpes simplex virus
  • Promoter activity
  • Reactivation

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Virology


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