A mutant deleted for most of the herpes simplex virus type 1 (HSV-1) UOL gene does not affect the spontaneous reactivation phenotype in rabbits

David Chan, Jacob Cohen, Julie Naito, Kevin R. Mott, Nelson Osorio, Ling Jin, Nigel W. Fraser, Clinton Jones, Steven L. Wechsler, Guey C. Perng

Research output: Contribution to journalArticle

5 Scopus citations


The mechanisms involved in the herpes simplex virus type 1 (HSV-1) latency-reactivation cycle are not fully understood. The latency-associated transcript (LAT) is the only HSV-1 RNA abundantly detected during neuronal latency. LAT plays a significant role in latency because LAT(-) mutants have a reduced reactivation phenotype. Several novel viral transcripts have been identified within the LAT locus, including UOL, which is located just upstream of LAT. The authors report here on a mutant, ΔUOL, which has a 437-nucleotide deletion that deletes most of UOL. ΔUOL replicated similarly to its wild-type parental McKrae HSV-1 strain in infected cells, the eyes, trigeminal ganglia, and brains of mice and rabbits. It was indistinguishable from wild-type virus as regards explant-induced reactivation in mice, and spontaneous reactivation in rabbits. In contrast, ΔUOL was significantly less virulent in mice. Thus, UOL appears to be dispensable for the wild-type reactivation phenotype while appearing to play a role in neurovirulence in ocularly infected animals.

Original languageEnglish (US)
Pages (from-to)5-16
Number of pages12
JournalJournal of neurovirology
Issue number1
Publication statusPublished - Feb 1 2006



  • HSV-1
  • LAT
  • Reactivation
  • UOL
  • Virulence

ASJC Scopus subject areas

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

Cite this