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

Journal of NeuroVirology - Tập 17 - Trang 546-551 - 2011
Nancy M. Sawtell1, Steven J. Triezenberg2, Richard L. Thompson3
1Department of Pediatrics, Division of Infectious Diseases, Cincinnati Children’s Hospital Medical Center, Cincinnati, USA
2Van Andel Research Institute, Grand Rapids, USA
3Department of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, USA

Tóm tắt

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.

Tài liệu tham khảo

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