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  • Title: Long-term persistence of defective HSV-1 vectors in the rat brain is demonstrated by reactivation of vector gene expression.
    Author: Starr PA, Lim F, Grant FD, Trask L, Lang P, Yu L, Geller AI.
    Journal: Gene Ther; 1996 Jul; 3(7):615-23. PubMed ID: 8818649.
    Abstract:
    Wild-type HSV-1 is known to persist indefinitely in neurons in the latent state; however, defective HSV-1 vectors, or amplicons, contain only approximately 1% of the HSV-1 genome and persistence of these HSV-1 vectors has not been studied even semiquantitatively in the adult rat brain. Defective HSV-1 vectors contain both an HSV-1 origin of replication and a packaging site, and in the presence of helper virus can undergo DNA replication and packaging into HSV-1 particles. Our prototype defective HSV-1 vector, pHSVlac, uses the HSV-1 immediate-early (IE) promoter to regulate expression of the Escherichia coli lacZ gene. Using cultured neuronal cells, we have previously shown that expression from pHSVlac can be augmented by superinfection with a helper virus. In this study, pHSVlac was delivered into the adult rat striatum or hippocampus, and 2-3 months after gene transfer we utilized superinfection with several replication-incompetent HSV-1 mutants to reactivate expression from pHSVlac in approximately 30% of the number of cells observed at 4 days after gene transfer. Thus, HSV-1 plasmid vectors can persist for at least 2-3 months in at least approximately 30% of the cells which are initially infected.
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