Isolation and Assay of Rabies Serogroup Viruses in CER Cells

Smith, Abigail L.; Tignor, Gregory H.; Mifune, Kumato; Motohashi, Tsunemasa

doi:10.1159/000148883

Cited by 89 publications

(38 citation statements)

References 5 publications

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“…CER (chick embryo-related) cells were grown at 37'~C in Eagle's MEM containing 1.2 g NaHCO3 per litre and supplemented with 10~ calf serum (Flow Laboratories), glutamine (2 mM), penicillin (100 U/ml) and streptomycin (100 lag/ml) as described by Smith et al (1977).…”

Section: Methodsmentioning

confidence: 99%

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Involvement of Gangliosides in Rabies Virus Infection

Superti

Hauttecoeur

Morelec

et al. 1986

Journal of General Virology

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SUMMARYThe role of gangliosides in rabies virus infection of chick embryo-related (CER) cells was investigated. Cultured cells were pretreated with neuraminidase to render the cells transiently non-susceptible to viral infection. Incubation of these desialylated cells with gangliosides allowed them to incorporate exogenous gangliosides and they recovered their susceptibility to rabies virus infection. Infection of CER cells was monitored by specific fluorescence 24 h after virus inoculation. The use of individual purified gangliosides or mixtures of two gangliosides to restore cellular susceptibility to viral infection showed that GTlb and GQlb were the most effective. The disialogangliosides were also active, principally GD 1 b, whereas GM 1, GM3 were poorly active and GD3 inactive. Incubation of rabies virus with gangliosides prior to virus infection reduced the percentage of infected cells. The results indicate that highly sialylated gangliosides are part of the cellular membrane receptor structure for the attachment of infective rabies virus. However, it is possible that other glycoconjugates such as glycoproteins or glycolipids also participate as components of a receptor structure for rabies virus.

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Section: Methodsmentioning

confidence: 99%

“…In this experimental model the infected cells were not of neuronal origin (Smith et al, 1977), and CER cells are susceptible to rabies virus infection without prior adaptation by serial passages. The next step would be to evaluate the role of gangliosides in the infection of neurons.…”

Section: Gm3mentioning

confidence: 99%

Involvement of Gangliosides in Rabies Virus Infection

Superti

Hauttecoeur

Morelec

et al. 1986

Journal of General Virology

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“…Titration of infectious virus. The concentration of infectious virus was determined on cultures of chick embryorelated cells as described by Smith et al (1977), with minor modifications. Briefly, the cells were grown in a medium containing NaHCO3 (1.2 g/l) and supplemented with 10% FCS, 2 mM-glutamine and antibiotics.…”

Section: Virusmentioning

confidence: 99%

The Anterograde Transport of Rabies Virus in Rat Sensory Dorsal Root Ganglia Neurons

Tsiang¹,

Lycke²,

Ceccaldi³

et al. 1989

Journal of General Virology

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SUMMARYWe have previously described the capacity of neurites extending from cultured rat sensory dorsal root ganglia (DRG) neurons to transport rabies virus through axoplasm in the retrograde direction. Here we report the infection of cultured neurons derived from the DRG and the subsequent anterograde transport of rabies virus from the infected cell somas through the extending neurites to its release into the culture supernatant. Viral transport was monitored by titration of the virus yield in the external compartment. Both early and late transport mechanisms of rabies virions were identified. The first one occurred a few hours post-infection and was undetectable 6 h later, before the initiation of viral replication. The velocity of this first wave of infective virions was in the range of 100 to 400 mm/day. The early viral transport was probably the result of a direct translocation of infective virions from the somatic site of entry to the neuritic extensions and subsequent release into the culture medium without replication in the cellular perikaryon. The second virus transport peak was detected 48 h post-infection. In this case, the virions detected in the neuritic compartment were presumably the progeny of the inoculated virus which had replicated in the perikaryon before the viral transport occurs. Using a four-compartment culture device we were able to demonstrate, simultaneously, retrograde and anterograde transport of the virus. The presence of antirabies serum in contact with the exposed neurites did not inhibit either the retrograde or the anterograde transport mechanisms. The viral release from the neuritic extensions after the fast anterograde transport was evaluated to be in the range of 150 to 300 infectious virions per bundle of neurites per day.

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“…The release of infectious virus into the culture medium, from infected cell lines, was titred by an in vitro plaque assay using Chicken Embryo Related (CER)cells, as described by Smith et al (1977).…”

Section: Titration Of Viral Infectivitymentioning

confidence: 99%

Ketamine-Mediated Inhibition of Rabies Virus Infection in vitro and in Rat Brain

Lockhart

Tsiang

Ceccaldi

et al. 1991

Antivir Chem Chemother

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SummaryThis report describes the effect of the dissociative anaesthetic ketamine, a non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, on the infectivity of the neurotropic rabies virus, in neuronal culture systems and in vivo. produced an approximate 10Q-1000-fold decrease in the production of rabies virus in neuronal cell cultures. Rabies virus infection was also inhibited in non-neuronal cell lines (Baby Hamster Kidney fibroblasts) but the inhibitory effects appeared better expressed in cells of neuronal origin (neuroblastoma and primary neuronal cultures). The kalnate/quisqualate competitive antagonist CNQX did not modify the course of rabies virus infection and modulators of known NMDA regulatory sites (Mg 2 + , Zn 2 + , HA-966) failed to antagonize the ketamine-rnediated inhibition of rabies virus production in neuroblastoma cells. Furthermore, Ca 2 +-mobilization does not appear to be involved because Ca 2 +-depleted and EGTA-treated medium did not affect the normal production of rabies virus. The action of ketamine on rabies virus infection in vivo was also investigated; peripheral treatment ofrats with this drug inhibited rabies virus infection in the thalamus, cortex and hippocampal formation (in particular the pyramidal layer of the CA1 region). Taken together, these data suggest that the ketamine-mediated inhibition of rabies virus production in vitro, although highly selective, is not acting via classic NMDA receptor-mediated mechanisms. However, the ketaminemediated retardation of rabies virus infection in vivo may offer new prospects for post-exposure rabies antiviral therapy.

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Isolation and Assay of Rabies Serogroup Viruses in CER Cells

Cited by 89 publications

References 5 publications

Involvement of Gangliosides in Rabies Virus Infection

Involvement of Gangliosides in Rabies Virus Infection

The Anterograde Transport of Rabies Virus in Rat Sensory Dorsal Root Ganglia Neurons

Ketamine-Mediated Inhibition of Rabies Virus Infection in vitro and in Rat Brain

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