Mapping herpes simplex virus type 1 latency-associated transcript sequences that protect from apoptosis mediated by a plasmid expressing caspase-8

W. Peng, L. Jin, G. Henderson, G. C. Perng, D. J. Brick, A. B. Nesburn, S. L. Wechsler, Clinton Jones

Research output: Contribution to journalArticle

25 Scopus citations


LAT (latency-associated transcript) is the only herpes simplex virus type 1 (HSV-1) transcript abundantly expressed during neuronal latency. LAT expression is required for the high reactivation phenotype of HSV-1 and this phenotype correlates with LAT's anti-apoptosis properties. LAT nucleotides 1 to 1499 inhibit caspase-8 (death receptor apoptotic pathway), but not caspase-9 (mitochondrial apoptotic pathway), -induced apoptosis as efficiently as larger LAT fragments. LAT sequences important for inhibiting caspase-8-induced apoptosis were also localized. The ability of LAT nucleotides 1 to 1499 to efficiently inhibit caspase-8-induced apoptosis correlates with the high reactivation phenotype of a mutant virus expressing just the first 1.5 kb of LAT (nucleotides 1 to 1499).

Original languageEnglish (US)
Pages (from-to)260-265
Number of pages6
JournalJournal of neurovirology
Issue number4
Publication statusPublished - Aug 1 2004



  • Caspase 8
  • HSV-1
  • Latency associated transcript
  • Reactivation from latency

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cellular and Molecular Neuroscience
  • Virology

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