Journal of NeuroVirology

, Volume 17, Issue 6, pp 546–551 | Cite as

VP16 serine 375 is a critical determinant of herpes simplex virus exit from latency in vivo

  • Nancy M. Sawtell
  • Steven J. Triezenberg
  • Richard L. Thompson


Development of novel prevention and treatment strategies for herpes simplex virus (HSV) mediated diseases is dependent upon an accurate understanding of the central molecular events underlying the regulation of latency and reactivation. We have recently shown that the transactivation function of the virion protein VP16 is a critical determinant in the exit from latency in vivo. HSV-1 strain SJO2 carries a single serine to alanine substitution at position 375 in VP16 which disrupts its interaction with its essential co-activator Oct-1. Here we report that SJO2 is severely impaired in its ability to exit latency in vivo. This result reinforces our prior observations with VP16 transactivation mutant, in1814, in which VP16 interaction with Oct-1 is also disrupted and solidifies the importance of the VP16–Oct-1 interaction in the early steps in HSV-1 reactivation.


Herpes simplex virus VP16 Latency Reactivation Exit from latency Phosphorylation Transactivation Mouse model 



This work was supported by Public Health Service NIH grants AI32121 to NMS and EY13168 to RLT.


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Copyright information

© Journal of NeuroVirology, Inc. 2011

Authors and Affiliations

  • Nancy M. Sawtell
    • 1
  • Steven J. Triezenberg
    • 2
  • Richard L. Thompson
    • 3
  1. 1.Department of Pediatrics, Division of Infectious DiseasesCincinnati Children’s Hospital Medical CenterCincinnatiUSA
  2. 2.Van Andel Research InstituteGrand RapidsUSA
  3. 3.Department of Molecular Genetics, Biochemistry, and MicrobiologyUniversity of Cincinnati College of MedicineCincinnatiUSA

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