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   <subfield code="a">The neuroinvasive profiles of H129 (herpes simplex virus type 1) recombinants with putative anterograde-only transneuronal spread properties</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Gregory Wojaczynski, Esteban Engel, Karina Steren, Lynn Enquist, J. Patrick Card]</subfield>
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   <subfield code="a">The use of viruses as transneuronal tracers has become an increasingly powerful technique for defining the synaptic organization of neural networks. Although a number of recombinant alpha herpesviruses are known to spread selectively in the retrograde direction through neural circuits only one strain, the H129 strain of herpes simplex virus type 1, is reported to selectively spread in the anterograde direction. However, it is unclear from the literature whether there is an absolute block or an attenuation of retrograde spread of H129. Here, we demonstrate efficient anterograde spread, and temporally delayed retrograde spread, of H129 and three novel recombinants. In vitro studies revealed no differences in anterograde and retrograde spread of parental H129 and its recombinants through superior cervical ganglion neurons. In vivo injections of rat striatum revealed a clear bias of anterograde spread, although evidence of deficient retrograde transport was also present. Evidence of temporally delayed retrograde transneuronal spread of H129 in the retina was observed following injection of the lateral geniculate nucleus. The data also demonstrated that three novel recombinants efficiently express unique fluorescent reporters and have the capacity to infect the same neurons in dual infection paradigms. From these experiments we conclude that H129 and its recombinants not only efficiently infect neurons through anterograde transneuronal passage, but also are capable of temporally delayed retrograde transneuronal spread. In addition, the capacity to produce dual infection of projection targets following anterograde transneuronal passage provides an important addition to viral transneuronal tracing technology.</subfield>
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   <subfield code="a">Springer-Verlag Berlin Heidelberg, 2014</subfield>
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   <subfield code="a">Herpes simplex virus</subfield>
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   <subfield code="a">Recombinants</subfield>
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   <subfield code="a">Fluorescent reporters</subfield>
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   <subfield code="a">Dual infection</subfield>
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   <subfield code="a">Wojaczynski</subfield>
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   <subfield code="u">Department of Neuroscience, University of Pittsburgh, 15260, Pittsburgh, PA, USA</subfield>
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   <subfield code="a">Engel</subfield>
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   <subfield code="u">Department of Molecular Biology and the Princeton Neuroscience Institute, Princeton University, 08544, Princeton, NJ, USA</subfield>
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   <subfield code="a">Patrick Card</subfield>
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   <subfield code="t">Brain Structure and Function</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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