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)

Six temperature-sensitive (ts) mutants of vesicular stomatitis virus (VSV) isolated from the central nervous system (CNS) following injection with ts G31 (III) all possessed a post-transcriptional defect, not found in the initial virus, that affects the stability of viral RNA transcripts. Examination of viral RNA metabolism in mouse neuroblastoma (N-18) cells revealed that RNA synthesis of the CNS isolates was decreased considerably at elevated temperatures (up to 80 or 90% at 39 degrees C). In addition, analysis of the RNA transcripts suggested that little if any normal-sized transcripts were made in cells infected with these CNS isolates at either 37 degrees C or 39 degrees C. The RNA deficiencies did not appear to be the result of a temperature-sensitive lability of virion transcriptase as examined by in vitro transcriptase assays. However, when N-18 cells infected with one of the CNS isolates, ts G31 BP, were first preincubated at the permissive temperature of 31 degrees C for 3 h and then shifted to 39 degrees C, RNA synthesis proceeded at a rate comparable to that of 31 degrees C. The viral mRNA species synthesized following the temperature shift also contained normal sized tracts of poly(A) RNA, suggesting that neither the viral transcriptase nor its polyadenylate synthetase was thermally labile. However, for any of the six CNS isolates, all species of viral RNA synthesized in cells that were first preincubated at 31 degrees C degraded rapidly when the cells were shifted to 39 degrees C. In contrast little or no RNA degradation of either 42S progeny RNA or mRNA species was detected in the wild-type VSV, ts G31 or three other VSV mutants that are defective in some aspect of viral RNA metabolism: [ts G11 (I), ts G22 (II), ts G41 (IV)]. The apparent phenotype alteration in the stability of viral RNA in all of these CNS isolates is discussed in terms of the possible genotypic changes that may have occurred as well a the unique CNS disease that accompanies infection by these viruses.
J Gen Virol 1981 Aug
PMID:RNA degradation defect in central nervous system isolates of vesicular stomatitis virus. 616 98

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.
J Gen Virol 1984 Oct
PMID:Comparative studies of rabies and Sindbis virus replication in human neuroblastoma (SYM-I) cells that can produce interferon. 620 14

Thirteen temperature-sensitive (ts) mutants of HSV-1 were analysed for their capacity to establish latent infections in the brains of mice. Eleven of the mutants could be classified as latency-positive or -negative; two could not be assigned to either group. Leakiness of mutants in the brain and differences in particle/infectivity ratios were found not to play a role in the results. Ts+ revertants of selected latency-negative mutants regained the capacity to establish latent infections, indicating that it was the ts lesion in these agents which was involved in latency. Ultrastructural studies of neuroblastoma cells infected with various mutants and maintained at the restrictive temperature showed that no absolute correlations could be made between capacity to establish latent infection and synthesis of various morphologically identifiable virus products. Finally, from a comparison of latency characteristics with previously established polypeptide phenotypes of mutants it was concluded that one immediate early and one or more later virus functions are necessary for establishment and/or maintenance of the latent state.
J Gen Virol 1980 Jul
PMID:Latency competence of thirteen HSV-1 temperature-sensitive mutants. 625 86

We report for the first time the replication of infectious adeno-associated virus type 1 (AAV-1) in rodent cells [primary mouse kidney (PMK) and mouse L929 cells] using murine adenovirus (MAV) as a helper virus and also the production of AAV-I virus antigen by herpes simplex virus type I (HSV-I) with its temperature-sensitive mutant ts 200 in mouse neuroblastoma (NB) cells. The infectious AAV virions produced by MAV on L cells had a buoyant density of 1.41 2ml in caesium chloride gradients.
J Gen Virol 1980 Nov
PMID:Properties of adeno-associated virus (type 1) replicated in rodent cells by murine adenovirus. 625 36

We have studied the effect of local anesthetics QX 572, which is permanently charged, and benzocaine, which is neutral, on batrachotoxin-activated sodium channels in mouse neuroblastoma N18 cells. The dose-response curves for each drug suggest that QX 752 and benzocaine each act on a single class of binding sites. The dissociation constants are 3.15 X 10(-5) M for QX 572 and 2.65 X 10(-4) M for benzocaine. Equilibrium and kinetic experiments indicate that both drugs are competitive inhibitors of batrachotoxin. When benzocaine and QX 572 are present with batrachotoxin, they are much more effective at inhibiting Na+ flux than would be predicted by a one-site model. Our results indicate that QX 572 and benzocaine bind to separate sites, each of which interacts competitively with batrachotoxin.
J Gen Physiol 1981 Feb
PMID:Local anesthetics QX 572 and benzocaine act at separate sites on the batrachotoxin-activated sodium channel. 626 60

Morphological changes were extensive following infection of murine neuroblastoma N-18 cells with a temperature-sensitive (ts) mutant of vesicular stomatitis virus (VSV), G31 (complementation group III), and incubation at 39 degrees C, a non-permissive condition for virion maturation. Incubation for 24 h after infection resulted in extensive morphological degeneration of mitochondria with over 80% from that in uninfected cells. Janus green B supravital staining, was reduced by 81% from that in uninfected cells. Cellular ATP levels were reduced by 50% 12 h after infection. Mitochondrial degeneration still occurred in infected cells after the inactivation of lysosomes with chloroquine. Extensive cell fusion and cytoplasmic vacuole formation also occurred during the non-permissive infection with ts G31. Loss of plasma membrane integrity was not the cause of vacuole formation since 90% of the cells were able to exclude trypan blue 24 h after infection, nor were the vacuoles the result of inactivation of the mitochondria since cyanide-poisoned cells did not form vacuoles. The cytopathic alterations observed in N-18 cells during the non-permissive infection of N-18 cells with ts G31 did not occur during the non-permissive infection of N-18 cells with ts G11 (I), ts G41 (IV), or u.v.-inactivated ts G31. However, the non-permissive infection with ts O45 (V) led to mitochondrial degeneration and cytoplasmic vacuole formation, but no cell fusion occurred. These results are discussed in light of the ultrastructural features previously observed in the central nervous system of mice infected with ts G31 and cells in culture infected with wild-type VSV.
J Gen Virol 1981 Aug
PMID:Cytopathic effects in mouse neuroblastoma cells during a non-permissive infection with a mutant of vesicular stomatitis virus. 627 Feb 68

Addition of 50 micrograms/ml chloroquine to neuroblastoma cells 1 h before infection with temperature-sensitive mutant ts G31 (III) of vesicular stomatitis virus (VSV) prevented virus-induced cell fusion from occurring. Interestingly, addition of chloroquine after infection still inhibited cell fusion. Based on the number of fusion events required to produce the polykaryocytes observed, cell fusion was inhibited 92% when chloroquine was added 1 h post-infection and 77% when chloroquine was added 2 h post-infection. The inhibition of virus-induced cell fusion could not be accounted for by an inhibition of virus protein synthesis because the virus protein synthesis measured 6 h post-infection was 90% of that in untreated, infected cells with chloroquine added 1 h post-infection, and the same as untreated, infected cells when chloroquine was added 2 h post-infection. No virus proteins were made, however, when chloroquine was added before infection, which is consistent with a chloroquine-mediated inhibition of virus uncoating. The release of infectious virions was completely inhibited when chloroquine was added before infection or 1 or 2 h post-infection, which indicated an inhibition of virus maturation in the later stages of virus assembly. By indirect immunofluorescence the virus glycoprotein (G protein) could not be detected on the surface of chloroquine-treated, infected cells, but the G protein was present inside the treated cells. With 125I-labelled anti-G protein IgG, 16% of the G protein found on the surface of untreated, infected cells was on the cell surface when chloroquine was added 2 h post-infection. When chloroquine was removed from infected cells, the G protein accumulated at the cell surface, and this accumulation could not be prevented by tunicamycin, an inhibitor of glycosylation. Furthermore, galactose was incorporated into the G protein in the presence of chloroquine. Therefore, the VSV G protein was being synthesized and glycosylated in the presence of chloroquine but the drug prevented the expression of the glycoprotein at the cell surface during the final stages of G protein assembly.U
J Gen Virol 1982 Sep
PMID:Inhibition of vesicular stomatitis virus glycoprotein expression by chloroquine. 629 May 97

Molecular and host range properties of the virulent L10 strain of Semliki Forest virus were compared to those of the avirulent A7 strain. No difference could be detected between the two strains in adsorption, nucleocapsid synthesis, protein synthesis, ratio of 42S:26S RNA, particle infectivity, interferon induction and susceptibility, or defective interfering particle production. A7 showed lower total RNA synthesis than L10 in BHK, G26-24 (oligodendroglioma) and C1300 (neuroblastoma) cells. Cytopathogenicity of A7 was reduced compared to L10 in C1300 cells but not in G26-24 cells. It is concluded that the avirulent A7 strain has similar host range and molecular properties to the neurovirulence mutants M9 and M136, and that demyelination may be produced by a similar mechanism.
J Gen Virol 1983 Jun
PMID:The avirulent A7 Strain of Semliki Forest virus has reduced cytopathogenicity for neuroblastoma cells compared to the virulent L10 strain. 685 73

Two strains of fixed rabies virus were examined for their ability to regenerate defective interfering (DI) particles and for possible correlation of DI particle production with the expression of virulence. A plaque-purified stock of the attenuated ERA strain (ERApp), which characteristically caused an auto-interfering death response in adult mice inoculated i.c., was serially passed at a high m.o.i. inBHK-21 cells. By the sixth passage, DI particles were regenerated that corresponded in sedimentation velocity and DI/RNA size to the smallest of three sizes of DI particles produced by the parental stock virus. The regeneration of ERA DI particles in vivo was not detected during 15 serial high or low m.o.i. passages of infected newborn mouse brain, though the passaged virus consistently elicited an auto-interfering-type death response when assayed in adult mice. The attenuated Flury HEPpp strain regenerated up to three unique size classes of DI particles during serial passage in BHK-21 or murine neuroblastoma C1300 clone NA cells compared with the one band of DI particles produced by the parental Flury HEP stock virus. The BHK-21 cell-adapted Flury HEPpp virus failed to kill adult mice when inoculated at high concentrations after two serial passages in NA cells. However, the virus became fully virulent and a single band of regenerated DI particles was visible. Additional bands of defective particles were visible following the third serial passage in NA cells. Single-stranded RNA with a mol. wt. of 0.62 x 10(6) was extracted from the first DI particle population to be regenerated. This corresponded in mol. wt. to the DI/ssRNA characteristic of the parental attenuated Flury HEP virus. However, in the parental type DI/RNA, partially dsRNA could be isolated in addition to ssRNA. Double-stranded RNA could not be detected in the regenerated DI particles derived from the virulent NA cell-propagated Flura HEPpp virus. These results suggest that the virulence phenotype of fixed rabies viruses does not depend on the presence or absence of DI particles.
J Gen Virol 1980 Nov
PMID:Regeneration of DI particles of virulent and attenuated rabies virus: genome characterization and lack of correlation with virulence phenotype. 746 9

1. SH-SY5Y, an adrenergic human neuroblastoma cell line, was used to examine the hypothesis that D-lysergic acid (LSD) affects the metabolism of microtubule-associated tau protein, thus affecting microtubule assembly and the transport of neurotransmitters. 2. After 48 hr treatment LSD (10(-5) and 10(-7) M) decreased 50 kDa tau protein in the membrane (pellet) fraction. The drug (10(-5) M) also decreased in the cytoplasmic (supernatant) fraction. 3. This reduction in tau protein was accompanied by a 65% increase (P < 0.05) in total protein after LSD (10(-7) M) in the cytoplasmic fraction.
Gen Pharmacol 1995 Sep
PMID:D-lysergic acid reduces microtubule-associated tau protein in SH-SY5Y human neuroblastoma cells. 755 48


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