Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dot hybridization was used to detect specific rabies RNA in brains, either from experimental infection in mouse or from brain material to be processed for routine diagnosis. 32P cDNA probes were employed to identify minute amounts of specific viral RNA. Purified RNA was obtained after phenol extraction. The RNA was fixed on nylon membranes and hybridized with a pool of M13 inserts complementary to 200-400 nucleotides of each rabies gene and mRNA. Hybridized, labelled probes were detected by autoradiography. There was strong cross-hybridization between fixed rabies and street rabies virus RNA, which enable the detection of field strains for diagnosis purpose using a fixed rabies (PV strain) cDNA. A positive response was obtained with as little as 80 ng of brain RNA material from a fixed rabies-infected mouse. Detection of viral RNA was still specific 1 week after death, the brain material being left at room temperature. A total correlation was found when the samples were examined in parallel using a fluorescent rabies-specific antibody and by virus isolation on murine neuroblastoma cells. These data show that the use of rabies-specific cDNA probes in a dot-blot hybridization assay has great potential for the diagnosis of rabies.
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PMID:Rapid diagnosis of rabies infection by means of a dot hybridization assay. 338 Jan 7

A Rapid Rabies Enzyme Immuno-Diagnosis (RREID) technique has been developed. This technique for the diagnosis of rabies was performed in microplates which had been previously sensitized with IgG to purified antinucleocapsids. Suspensions of homogenized material were incubated in the plate and the specific binding of rabies antigen was revealed by the use of the same IgG conjugated with peroxidase. With the RREID technique it was possible to detect rabies antigens in brain specimens with the same specificity and sensitivity as that of the direct immunofluorescence test or the neuroblastoma cell inoculation technique regardless of the species of animal from which the specimen was derived. Moreover, RREID was performed with fox salivary gland specimens with the same results as were obtained with brain specimens. RREID does not require an UV light microscope and a photometer is not essential. It is a useful and simple technique for the routine laboratory diagnosis of rabies.
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PMID:A rapid rabies enzyme immuno-diagnosis (RREID): a useful and simple technique for the routine diagnosis of rabies. 353 Dec 15

Although the cell-to-cell spread of many viruses in vitro is inhibited by antibody, the effect of antibody on such spread of rabies viruses is uncertain. Thus, we examined the effects of anti-rabies virus immune sera and monoclonal antibodies (MAbs) on the in vitro spread of pathogenic rabies viruses in neuronal and nonneuronal cells. Both anti-rabies virus immune sera and neutralizing antiglycoprotein MAbs inhibited the cell-to-cell spread of street rabies virus, challenge virus standard, and ERA rabies viruses in cultures of neuroblastoma cells and of nonneuronal BHK-21 and chicken embryo-related cells. Furthermore, the cell-to-cell spread of virus was inhibited by greater than or equal to 75% with less than 1 IU/ml of human antirabies immunoglobulin. Nonneutralizing antinucleocapsid MAbs did not inhibit viral spread. After the immune serum was removed from the monolayers, virus spread rapidly to uninfected cells. Thus, antibody controlled the cell-to-cell spread of the virus but did not eliminate it from the cultures. Because antibody was more effective in inhibiting viral spread in fibroblast and epithelioid cells than in neuroblastoma cells infected at a high multiplicity of infection, we suggest that the inhibition of viral cell-to-cell spread by antibody in vivo would more likely occur at an initial site of exposure and before nerves are infected.
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PMID:Immune sera and antiglycoprotein monoclonal antibodies inhibit in vitro cell-to-cell spread of pathogenic rabies viruses. 362 41

A cell culture infection test was developed for the isolation of rabies virus from field cases submitted for rabies diagnosis. The procedure involved the addition of a suspension of suspect brain tissue to a suspension of murine neuroblastoma cells in 96-well microtiter plates. The cultures were then incubated at 35-36 degrees C for four days at which time they were fixed, stained with a fluorescein-labelled hamster antirabies antibody conjugate and examined with a fluorescence microscope. Rabies antigen in cells was readily visible as brilliant, apple-green fluorescent particles. This technique was compared with the standard mouse inoculation test and was at least as sensitive to infection with small amounts of virus, required a much shorter test period and was substantially more economical than the mouse inoculation test. The new cell culture test is now in use at this laboratory, replacing the mouse inoculation test.
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PMID:A tissue culture infection test in routine rabies diagnosis. 365 91

Pathogenic parental rabies virus and apathogenic variant virus were shown to differ in their ability to infect neurons in vivo and neuroblastoma cells in vitro. After intracerebral inoculation, the distribution of infected neurons in the brain was similar for both viruses, but the rate of spread throughout the brain, the number of infected neurons, and the degree of cellular necrosis were much lower in the case of apathogenic virus. After adsorption to mouse neuroblastoma cells, apathogenic virus was less rapidly internalized than pathogenic virus, and cell-to-cell spread of apathogenic variant virus was completely prevented by the addition of rabies virus-neutralizing antibody, whereas the spread of pathogenic virus was not affected.
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PMID:Differences in cell-to-cell spread of pathogenic and apathogenic rabies virus in vivo and in vitro. 389 71

Chick embryo fibroblast-passaged Flury high egg passage (HEP) rabies virus failed to kill nude mice or cyclophosphamide-treated mice when inoculated intracerebrally. The virus regained neurovirulence for adult mice after three passages in mouse neuroblastoma C1300 cells (NA cells). However, even after 20 passages in NA cells, the virulence could not be increased to the level shown by the virus passaged several times in suckling mice. Some physiological and biological properties of the virus showing and not showing mouse virulence after five serial passages and after one single passage in NA cells, respectively, were compared.
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PMID:Virulence of chick embryo fibroblast-passaged flury HEP rabies virus and its revertants in mice. 390 72

Apparent interferon-mediated persistent infection of rabies virus (HEP-Flury strain) was established in a human neuroblastoma SYM-I (clone K-104) cell line, which had the ability to produce interferon. This infection produced variable but small amounts of progeny virus and interferon (up to 100 IU/ml), and resisted superinfection with vesicular stomatitis virus (VSV) and Sindbis virus as well as homologous rabies virus. The treatment of this infection with anti-interferon antibody stimulated virus replication and extensive c.p.e. However, some cells survived and grew rapidly without any sign of c.p.e. These produced increased amounts (100 to 1000 times) of infectious and DI particles in the presence of anti-interferon antibody, becoming susceptible to superinfection with VSV but remaining resistant to the original rabies virus. Small plaque mutants appeared and replaced the original virus during the long-term cultivation of the persistent infection. Several mutants tested were all identified as Sdi (DI-resistant) mutants, suggesting that the persisting viruses were endowed by the Sdi mutation with a selective advantage over the original virus even in interferon-mediated persistent infections.
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PMID:Persistent infection of rabies virus (HEP-Flury strain) in human neuroblastoma cells capable of producing interferon. 399 11

Acute and persistent rabies virus infection of mouse neuroblastoma-rat glioma hybrid cells (NG-108-15) results in a loss of the normal inhibiting function of opiates via the opiate receptor on hormone-stimulated adenylate cyclase activity. Previous studies of these persistently infected cells have shown a decrease in the affinity of the opiate receptors for agonists without any change in the number of these receptors. We now demonstrate that persistently infected cells are unable to couple the opiate receptors to the inhibitory regulatory protein Ni of the adenylate cyclase, as measured by the loss of stimulation of the GTPase activity of this protein. However, the unstimulated basal GTPase activities of the regulatory components Ni and Ns are unchanged in the persistently infected cells. These studies also reveal a disorder of the stimulation of the adenylate cyclase by GTP or fluoride via the stimulating regulatory G/F protein (Ns) in persistently infected cells, whereas direct stimulation of the catalytic subunit of the adenylate cyclase by forskolin remains unchanged. Therefore, there are different points of dysfunction caused by the persistent rabies infection in the signal pathway from the opiate receptor to the adenylate cyclase and from the stimulating Ns protein to the enzyme: (i) opiate receptor binding is reduced by a decrease of agonist affinity (previously published data), (ii) the stimulation of GTPase activity of the inhibiting regulatory component Ni of the adenylate cyclase system is inhibited, and (iii) the signal pathway from the stimulating regulatory component of the adenylate cyclase system to the unchanged activity of the catalytic subunit is defective.
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PMID:Inhibition of opiate receptor-mediated signal transmission by rabies virus in persistently infected NG-108-15 mouse neuroblastoma-rat glioma hybrid cells. 614 55

Two lysosomotropic agents, ammonium chloride and chloroquine inhibit the infection of murine neuroblastoma cells by rabies virus. The experiments indicate that rabies virus infects the neuronal cells through an endosome pH dependent entry pathway.
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PMID:Ammonium chloride and chloroquine inhibit rabies virus infection in neuroblastoma cells. Brief report. 614 53

K-104 cells, a cloned cell line derived from a human neuroblastoma (SYM-I), were induced by rabies HEP-Flury virus to release large amounts of interferon, and the resulting antiviral activity significantly suppressed the rabies virus replication. The role of endogenous interferon was confirmed by treatment with anti-interferon antibody which increased the yield of progeny virus. The virus yield in the second undiluted passage through K-104 cells was much less than that in the first passage, because of the antiviral state initiated by brief contact of interferon present in the virus inoculum with cells during the short period of virus adsorption. When the m.o.i. was relatively low, as in the third undiluted passage, the effect of interferon present in the inoculum was enhanced and most of the infected cells survived but were shown to be in a state of persistent infection. Defective interfering (DI) particles did not accumulate rapidly during these three undiluted passages. When Sindbis virus was used for infection, the endogenous interferon system of K-104 cells was not activated during 12 undiluted passages. However, on the 12th passage, the yield began to decline due to the generation and accumulation of DI particles.
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PMID:Comparative studies of rabies and Sindbis virus replication in human neuroblastoma (SYM-I) cells that can produce interferon. 620 14


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