Two α-herpesvirus strains are transported differentially in the rodent visual system

Card, J. Patrick; Whealy, M. E.; Robbins, A. K.; Moore, Robert Y.; Enquist, Lynn W.

doi:10.1016/0896-6273(91)90236-s

Cited by 211 publications

(216 citation statements)

References 53 publications

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“…the olfactory, trigeminal, sympathetic and parasympathetic pathways (Babic et al, 1996). These results confirm and extend observations from other laboratories that PrV or HSV-1 gE is implicated in transneuronal transfer rather than in penetration and multiplication in first order neurons (Card et aL, 1992;Ba[an et aI., 1994;Kritas et al, 1994, Mulder et a]., 1994Dingwell et al, 1995;Standish et al, 1994).…”

Section: Introductionsupporting

confidence: 80%

Glycoprotein gH of Pseudorabies Virus is Essential for Penetration and Propagation in Cell Culture and in the Nervous System of Mice

Babic

Klupp

Makoschey

et al. 1996

Journal of General Virology

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Glycoprotein H (gH) of pseudorabies virus (PrV)is a structural component of the virion and forms a complex with another glycoprotein, gL. For a detailed analysis of the function of PrV gH, we isolated a gH-deficient mutant on transcomplementing gH-expressing cells after insertion of a p-galactosidase expression cassette into a partially deleted gH gene. The absence of gH did not affect primary or secondary attachment of PrV but the mutant was not infectious. The defect in infectivity could partially be overcome by experimentally induced membrane fusion using PEG, which suggests that gH was necessary for fusion between virion and cellular membranes. After intranasal inoculation into mice, the LDso of complemented gH PrV was more than four orders of magnitude higher than that of wild-type PrV. Infection of the respiratory epithelium was much less efficient with complemented gH PrV as compared with rescued PrV, reflecting the lack of direct cell-to-cell spread. Complemented gH PrV was able to penetrate into a few trigeminal and sympathetic first order neurons accessible from the nasal cavity, whereas transneuronal transfer in the second order neurons was not observed. In summary, gH is essential for entry and cell-to-cell spread in cell culture, and for propagation in the nervous system of mice. This substantiates the hypothesis that transneuronal spread in vivo and direct cell-to-cell spread in cell culture are governed by similar mechanisms.

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Section: Introductionsupporting

confidence: 80%

Glycoprotein gH of Pseudorabies Virus is Essential for Penetration and Propagation in Cell Culture and in the Nervous System of Mice

Babic

Klupp

Makoschey

et al. 1996

Journal of General Virology

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“…Previous studies have shown that neurotropic viruses can initiate infection in the periphery and can move through peripheral neurons to reach the central nervous system (Card et al, 1991;Ohka et al, 1998;Samuel et al, 2007;Tyler et al, 1986). Therefore, we hypothesized that mice with neurotropic disease may have higher viral titres in peripheral neurons and brain.…”

Section: Yfv-17d Titres In Ifnar "/" Micementioning

confidence: 98%

Spectrum of disease outcomes in mice infected with YFV-17D

Erickson

Pfeiffer

2015

Journal of General Virology

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“…The Bartha strain of PRV (a generous gift from Dr. Lynn Enquist, Princeton University) was used for all experiments that involved virus injections. The Bartha strain is an attenuated strain of PRV that reliably labels various neural pathways via transneuronal transport, including visual (Card et al, 1991), autonomic (Card et al, 1990;Strack and Loewy, 1990), and somatic pathways (Martin and Dolivo, 1983;Rouiller et al, 1986;Jasmin et al, 1997). The titer of the virus was 1 ϫ 10 8 pfu/ml of culture medium.…”

Section: Methodsmentioning

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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Two α-herpesvirus strains are transported differentially in the rodent visual system

Cited by 211 publications

References 53 publications

Glycoprotein gH of Pseudorabies Virus is Essential for Penetration and Propagation in Cell Culture and in the Nervous System of Mice

Glycoprotein gH of Pseudorabies Virus is Essential for Penetration and Propagation in Cell Culture and in the Nervous System of Mice

Spectrum of disease outcomes in mice infected with YFV-17D

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

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