A speculated ribozyme site in the herpes simplex virus type 1 latency-associated transcript gene is not essential for a wild-type reactivation phenotype

Dale Carpenter, Sukhpreet Singh, Nelson Osorio, Chinhui Hsiang, Xianzhi Jiang, Ling Jin, Clinton Jones, Steven Wechsler

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

During herpes simplex virus-1 (HSV-1) latency in sensory neurons, LAT (latency-associated transcript) is the only abundantly expressed viral gene. LAT plays an important role in the HSV-1 latency-reactivation cycle, because LAT deletion mutants have a significantly decreased reactivation phenotype. Based solely on sequence analysis, it was speculated that LAT encodes a ribozyme that plays an important role in how LAT enhances the virus' reactivation phenotype. Because LAT ribozyme activity has never been reported, we decided to test the converse hypothesis, namely, that this region of LAT does not encode a ribozyme function important for LAT's ability to enhance the reactivation phenotype. We constructed a viral mutant (LAT-Rz) in which the speculated ribozyme consensus sequence was altered such that no ribozyme was encoded. We report here that LAT-Rz had a wild-type reactivation phenotype in mice, confirming the hypothesis that the speculated LAT ribozyme is not a dominant factor in stimulating the latency-reactivation cycle in mice.

Original languageEnglish (US)
Pages (from-to)558-562
Number of pages5
JournalJournal of neurovirology
Volume14
Issue number6
DOIs
StatePublished - 2008

Keywords

  • Herpes simplex virus
  • LAT
  • Latency
  • Reactivation
  • Ribozyme

ASJC Scopus subject areas

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

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