Binding, uptake and retrograde axonal transport of herpes virus suis in sympathetic neurons

Marchand, C.; Schwab, Martin E.

doi:10.1016/0006-8993(86)90024-7

Cited by 49 publications

(42 citation statements)

References 17 publications

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“…For example, some neurotropic viral pathogens, such as poliovirus, enter axons by endocytosis and subsequently traverse the axon in the endosome (25). However, by transmission electron microscopy (TEM), herpesvirus capsids are typically observed directly in the cytosol subsequent to entry into axons (15,26,27). Similarly, we see membrane-free capsids in axons in our culture model by TEM (data not shown).…”

Section: Discussionmentioning

confidence: 64%

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Smith

Pomeranz

Gross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

132

177

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The core structures of many viruses move within cells by association with host cytoskeletal motor proteins; however, the mechanisms by which intracellular viral particles are transported toward sites of replication or the cell periphery at distinct stages of infection remain to be understood. The regulation of herpesvirus directional transport in sensory neurons was examined by tracking individual viral capsids within axons at multiple frames per s. After entry into axons, capsids underwent bidirectional and saltatory movement to the cell body independently of endosomes. A comparison of entry transport to a previous analysis of capsid axonal transport during egress revealed that capsid targeting in and out of cells occurs by modulation of plus-end, but not minus-end, motion. Entry transport was unperturbed by the presence of egressing virus from a prior infection, indicating that transport direction is not modulated globally by viral gene expression, but rather directly by a component of the viral particle.virus ͉ neuron

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Section: Discussionmentioning

confidence: 64%

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Smith

Pomeranz

Gross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

132

177

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“…Once injected, the virus particles would not persist in the extracellular space but would enter cells by fusion of the viral membrane with the axon terminal and perikaryon cytoplasmic membrane (Marchand and Schwab, 1986;Card and Enquist, 1995). In neurons, the virus is retrogradely transported to the nucleus of the cell, losing its tegument and capsid (Roizman and Furlong, 1974;Spear, 1993;Card and Enquist, 1995).…”

Section: Discussionmentioning

confidence: 99%

Transneuronal Labeling of a Nociceptive Pathway, the Spino-(Trigemino-)Parabrachio-Amygdaloid, in the Rat

et al. 1997

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Transneuronal tracing of a nociceptive pathway, the spino-(trigemino)-parabrachio-amygdaloid pathway, was performed using an ␣-herpes virus, the Bartha strain of pseudorabies virus (PRV). Microinjection of PRV into the central nucleus of the amygdala (Ce) resulted in progressive retrograde and transneuronal infection of a multisynaptic circuit involving neurons in the brainstem and spinal cord as detected immunocytochemically. At short survival (26 hr), retrogradely labeled neurons were concentrated in the external lateral nucleus of the parabrachial complex (elPB) but were absent from both the trigeminal nucleus caudalis (TNC) and the spinal cord. At longer survivals (52 hr), labeled cells were present in lamina I of both the TNC and spinal dorsal horn. Retrograde labeling from the Ce with Fluorogold demonstrated that elPB neurons have long dendrites extending laterally into the terminal field of spinal and trigeminal afferents, where transneuronal passage of PRV to these afferents could occur. Even longer survivals (76 hr) resulted in a columnar pattern of cell labeling in the TNC and spinal dorsal horn that extended from lamina I into lamina II. At this longest survival, primary sensory neurons became infected. Bilateral excitotoxic lesions of the elPB blocked almost all viral passage from the Ce to superficial laminae of the TNC and spinal dorsal horn. These results demonstrate that nociceptive input to the amygdala is relayed from neurons in lamina I through the elPB. We propose that this modular arrangement of lamina I and II neurons may provide the basis for spinal processing of peripheral input to the amygdala. Key words: pain pathways; amygdala; superficial dorsal horn; parabrachial nucleus; spinal processing; viral tracer; PRV; pseudorabies virusThe central nucleus of the amygdala (Ce) is the terminal area of a major ascending nociceptive pathway, the spino-(trigemino)-parabrachio-amygdaloid tract . Most Ce neurons respond to noxious, but not innocuous, stimuli (Bernard and Besson, 1990;. The main source of afferents to the Ce is the external lateral parabrachial nucleus (elPB) (Saper, 1995). Previous anatomical studies have, however, failed to demonstrate a significant projection from the spinal dorsal horns and trigeminal nucleus caudalis (TNC) to the elPB (Blomqvist et al., 1989). Rather, afferents from nociceptive regions of the dorsal horn, laminae I and V, terminate in nuclei located in the lateral parabrachial area surrounding the elPB, none of which project to the amygdala (Bernard et al., 1995;Feil and Herbert, 1995;Saper, 1995).To explain this discrepancy, it has been proposed that elPB neurons might have long dendrites that extend into the external nuclear layer where spinal and trigeminal afferents terminate (Blomqvist et al., 1989;Saper, 1995). There is ultrastructural evidence that spinal and trigeminal afferents contact amygdala projection neurons in the lateral parabrachial area (Ma and Peschanski, 1988), but in this study, neither the laminae of origin of the spinal and trigeminal neur...

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“…However, HSV-1 and HSV-2 demonstrated equal binding in mouse glial cell preparations. Pseudorabies virus uptake and retrograde transport studies have reported the presence of limited viral specific receptors on axon terminals which mediate viral uptake (Marchand and Schwab, 1986). These findings suggest preferential infectivity at the synapse, but also illustrate that host species type, viral strain and different cell types influence the path of infection.…”

Section: A Tool For Transneuronal Tracing Studiesmentioning

confidence: 95%

“…In HSV infected neurons, nucleocapsids have been observed obtaining a primary envelope at the inner lamina of the nuclear membrane. Virions are subsequently released into the endoplasmic reticulum as naked nucleocapsids by a de-envelopment fusion with the outer nuclear membrane (Marchand and Schwab, 1986;Lycke et al, 1988). HSV nucleocapsids receive a secondary envelopment by the endoplasmic reticulum and follow anterograde transport to the cellular membrane by a transport vesicle.…”

Section: A Tool For Transneuronal Tracing Studiesmentioning

confidence: 99%

The roles of herpes simplex virus in neuroscience

Turner¹,

Jenkins²

1997

J Neurovirol

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Herpes simplex virus (HSV) has been a focus of research in many laboratories during the last 30 ± 35 years, with the majority centered on the virus' replication, molecular biology and pathogenesis. Recently, HSV has begun to receive considerable attention in the field of neuroscience, where scientists have begun to use the virus as a tool or model for several areas of investigation. These areas include the construction and development of HSV-based vectors for gene therapy and the use of HSV as a neuronal tracer, as a model for demyelinating disease and to study interactions between the nervous, immune and endocrine systems. The goal of this paper is to review these different roles for HSV in the broad field of neuroscience.

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Binding, uptake and retrograde axonal transport of herpes virus suis in sympathetic neurons

Cited by 49 publications

References 17 publications

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Transneuronal Labeling of a Nociceptive Pathway, the Spino-(Trigemino-)Parabrachio-Amygdaloid, in the Rat

The roles of herpes simplex virus in neuroscience

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