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Jennifer LaVail, Jolene Draper, Graham Stephenson, Guiqing Huang, Andrea Bertke, Daniel Cortez; Delivery of Herpes Simplex Virus DNA to Retinal Ganglion Cell Axon is Dependent on Viral Protein Us9. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1730.
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© ARVO (1962-2015); The Authors (2016-present)
The pathogenic spread of neurotropic virus relies on axonal transport of viral DNA. The role of the Herpes Simplex Virus (HSV) protein Us9 in viral intracellular spread is contentious. We compared the results of Us9 deletions in two HSV strains using a novel quantitative assay to test the hypothesis that Us9 regulates the delivery of viral DNA to the distal axon of retinal ganglion cells in vivo. We also deleted a nine amino acid motif in the Us9 protein of F strain (Us9-30) to define the role of this domain in DNA delivery.
The vitreous chambers of murine eyes were infected with equivalent amounts of F or NS strains of HSV. At three, four or five days post infection (dpi) both optic tracts (OT) were dissected and viral genome was quantified by qPCR.
At three dpi the F strain Us9- and Us9-30 mutants delivered less than 10% and 1%, respectively, of the viral DNA delivered after infection with the Us9R (control) strain. The effect of the deletion of Us9 was less severe in the NS Us9 deletion experiments. By four and five dpi delivery of viral DNA had partially recovered, although to a greater degree in NS as compared to F experiments.
A highly conserved acidic cluster within the Us9 protein plays a critical role for genome transport to the distal axon. The transport is less dependent on Us9 expression in the NS than in F strain virus suggesting compensatory roles for the NS variant. This assay can be used to compare transport efficiency in other neurotropic viral strains.
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