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The HSV 1 genome in quiescently infected NGF differentiated PC12 cells can not be stimulated by HSV superinfection
Journal article   Peer reviewed

The HSV 1 genome in quiescently infected NGF differentiated PC12 cells can not be stimulated by HSV superinfection

Ying-Hsiu Su, Michael Moxley, Rohini Kejariwal, Anand Mehta, Nigel W Fraser and Timothy M Block
Journal of neurovirology, v 6(4), pp 341-349
01 Aug 2000
PMID: 10951558

Abstract

This study reports that quiescent herpes simplex virus (HSV) type 1 genomes, persisting in long-term infected nerve growth factor (NGF) differentiated PC12 cells, were not stimulated by superinfection with a HSV-1. We have previously shown that HSV-1 can establish long term, quiescent infections in NGF differentiated PC12 cells. To determine if virion associated factors or virus induced gene products could trans-activate the quiescent viral genomes, long term infected PC12 cell cultures were superinfected at a high moi (moi of 20) with a recombinant HSV 17α47/lacZ that contains the lacZ gene within the alpha 47 locus. Progeny virus and gene expression from the resident 'quiescent' viral genomes were not detected following superinfection with recombinant 17α47/lacZ. The failure to stimulate the quiescent genome appears to be related to the inability of the super infecting virus to induce any gene expression from its own genome following entry into the long term NGF treated PC12 cells. Interestingly, both primary and superinfecting viruses could be stimulated from the quiescently infected cultures following cocultivation with inducer cells. These data suggest that (i) HSV genomes in quiescently infected PC12 cells are unable to be stimulated by incoming virion associated factors and (ii) NGF differentiated PC12 cells maintained in tissue culture for longer than 3 weeks became completely refractory to viral gene expression. The possibilities that these results are reflective of populations of neural cells, in vivo in mouse central nervous system, which are completely refractory to virus gene expression, yet accommodating to the maintenance of viral genomes and thus favor 'latency', are discussed.

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Collaboration types
Domestic collaboration
Web of Science research areas
Neurosciences
Virology
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