Format

Send to

Choose Destination
See comment in PubMed Commons below
J Neurovirol. 2011 Dec;17(6):546-51. doi: 10.1007/s13365-011-0065-y. Epub 2011 Dec 6.

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

Author information

1
Department of Pediatrics, Division of Infectious Diseases, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA. nancy.sawtell@cchmc.org

Abstract

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.

PMID:
22144074
PMCID:
PMC3269237
DOI:
10.1007/s13365-011-0065-y
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer Icon for PubMed Central
    Loading ...
    Support Center