Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relative susceptibility of neurons and glia, grown as monolayers in vitro, to rabies virus infection was explored. Established cell lines of neuronal or glial phenotype and primary cultures of cells derived from mouse dorsal root ganglia (DRC) or brain were used as homologues of the targets of rabies virus in the nervous system. Fixed rabies virus (CVS) strain was used in most experiments; other fixed rabies strains (PV, HEP, ERA) and a street rabies virus isolate were used in some. Virus-cell tropism was determined by immunofluorescence assay for rabies nucleocapsid antigen and cell permissivity was assessed by titration of virus yields. Neuronal cells always exhibited a much greater susceptibility to infection and a greater propensity to sustain viral growth. By immunofluorescence, 90-100% of neurons commonly had viral inclusion bodies, while doses of the virus three to four orders of magnitude higher still left greater than 99% of astrocytes, in brain cell cultures and 90 +/- 5% of the non-neuronal cells in DRG cultures without any obvious signs of rabies virus. Neuroblastoma cells (95 +/- 5% with viral antigens) produced viral yields about four orders of magnitude higher than glioma cells (10 +/- 5% with viral antigens). Though the overall infectivity of street virus was lower than that of fixed virus strains, a significantly higher viral tropism for neurons than for glia was maintained. Thus, primary neuronal cultures offer a means of exploring molecular events in rabies virus infection and their role in pathogenesis.
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PMID:Neurotropism of rabies virus. An in vitro study. 686 37

For the evaluation of residual pathogenicity of Flury HEP strain 675, the vaccinal virus was orally administered to 207 animals belonging to 15 wild-living and 1 domestic species. Rabies virus antigen could be demonstrated by FA method in 20 animals. Reisolation of the virus was possible from 23 animals within the first two weeks after application, the titres being very low. During the observation period of 100 days no symptoms of rabies could be observed in the animals tested.
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PMID:Safety tests with Flury HEP strain 675 in wild-living European mammals. 712 66

A group of 14 adult foxes was orally vaccinated with 2 ml Flury HEP strain 675, titre 10(8.2 TCID50. Each fox seroconverted neutralizing antibody titres ranging between 1:40 and 1:640. These foxes survived an intramuscular challenge with 8000 mouse LD50 pathogenic rabies virus, whereas six out of seven unprotected control foxes died within 28 days. This study was accompanied by virus isolation, fluorescence microscopic examination and neutralization tests.
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PMID:Effectivity of oral vaccination of foxes against rabies with Flury HEP strain 675. 712 67

The titres of rabies virus in the saliva of kudu are higher than those of the salivary glands. The high titres are an indication of active excretion and multiplication in tissues other than the salivary glands. Two out of 4 kudu died of rabies after experimental infection by the instillation of infected saliva onto their buccal and nasal mucosae. Mice and 2 cattle resisted a similar exposure. Kudu also developed antibodies against rabies after instillation of HEP Flury virus onto their nasal and buccal mucosae. Cattle did not react when they were treated in the same way. These results suggest a high susceptibility of kudu to rabies when the virus is applied to their mucous membranes.
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PMID:Non-bite transmission of rabies in kudu (Tragelaphus strepsiceros). 718 35

Mouse neuroblastoma (MNB) cells infected with ERA virus were specifically lysed in the presence of rabbit complement by antisera produced in mice to challenge virus standard (CVS), ERA, Flury HEP or street virus (SV) strains of rabies. MNB or EL-4 cells persistently infected with ERA, MNB cells infected with CVS, and BHK-21/S13 cells infected with ERA or Flury HEP also were suitable targets. CER cells infected with either ERA, CVS or Flury HEP, BHK-21/S13 cells infected with CVS and MNB cells infected with Flury HEP were not suitable targets. Two unusual findings indicated that 1. some cells which were greater than 80 percent positive for rabies viral membrane antigen(s) were poorly lysed, and 2. some cells that expressed cytoplasmic antigen lacked detectable membrane antigens.
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PMID:Influence of cell type and virus upon lysis of rabies virus-infected cells by antibody and complement. 733 91

Each of several strains of fixed rabies virus was found to replicate to high titers in C1300 mouse neuroblastoma (clone NA) cells, without adaptation. Rabies serogroup Lagos bat, Mokola, and Duvenhage viruses also replicated efficiently in NA cells. Kotonkan and Obodhiang viruses replicated efficiently after adaptation, to titers not previously obtained in vitro. Infection in NA cells was frequently more cytopathic than in BHK-21 cells, allowing titration of Kotonkan and Obodhiang viruses by plaque assay. Duvenhage virus caused syncytium formation. Serial propagation of rabies viruses at a high multiplicity of infection in NA cells led to a rapid decline in virus yields; similar "autointerference" has not previously been demonstrated with rabies virus in other cell systems. Rabies virus infection in NA cells exhibited extreme sensitivity to interference by experimentally added defective interfering virions. Although several strains of attenuated rabies virus consistently reverted rapidly to virulence after propagation in NA cells, other strains of attenuated rabies and rabies serogroup viruses acquired increased virulence at a more gradual rate or not at all, suggesting that diverse characters may control virulence. When attenuated Flury HEP rabies virus was serially propagated at a low multiplicity of infection in either NA cells or suckling mouse brain, virulence appeared at a very variable rate, indicating that these systems may selectively enhance replication of randomly occurring virulent virus mutants.
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PMID:Rabies serogroup viruses in neuroblastoma cells: propagation, "autointerference," and apparently random back-mutation of attenuated viruses to the virulent state. 738 May 49

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.
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PMID:Regeneration of DI particles of virulent and attenuated rabies virus: genome characterization and lack of correlation with virulence phenotype. 746 9

The glycoprotein gene of the rabies virus vaccine strain Vnukovo-32 was sequenced and the deduced protein sequence was analyzed and compared with that of various laboratory and street strains. The amino acid sequence homologies of strain Vnukovo-32 were compared with fixed strains ERA, SAD B19, PV, HEP-Flury, CVS and two street strains, canine and CXX89-1, were 98.9% (6 replacements), 98.3% (9), 96.2% (20), 91.4% (45), 87.0% (68), 93.5% (34) and 91.4% (45), respectively. Sequence alignments of the proteins revealed that the most conserved region is the ectodomain, whereas the transmembrane and cytoplasmic domains showed significant divergence.
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PMID:Nucleotide and deduced amino acid sequences of the glycoprotein gene of rabies virus vaccine strain Vnukovo-32. 797 81

We have established a murine hybridoma cell line RG719 which produces a rabies virus-neutralizing IgM-type monoclonal antibody (referred to as MAb RG719). Immunoblot analysis indicated that the antibody recognized a sequential epitope of G protein. Among four rabies virus strains tested, the antigenicity to MAb RG719 was absent from the Nishigahara strain, while the other three strains (HEP, ERA and CVS) reacted to the MAb. Studies with deletion mutants of the G protein indicated that the epitope was located in a middle region of the primary structure of G protein, ranging from position 242 to 300. By comparing the estimated amino acid sequence of the four strains, we found in this region two amino acids (at positions 263 and 291) which are common to three of those strains but are not shared by the Nishigahara strain. The site-directed point mutagenesis revealed that replacement of phenylalanine-263 by leucine destroyed the epitope of the HEP G protein, while the epitope was generated on the Nishigahara G protein whose leucine-263 was replaced by phenylalanine. These observations suggest that phenylalanine-263 is essential for constructing the epitope for MAb RG719. The synthetic 20-mer peptide produced by mimicking the amino acid sequence (ranging from amino acid positions 249 to 268) of the presumed epitope region was shown to bind specifically to MAb RG719 and also to raise the virus-neutralizing antibodies in rabbits. Vaccination with the HEP vaccine produced in Japan induced in humans and rabbits production of significant amounts of the antibodies which reacted with the 20-mer peptide.
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PMID:Mapping and characterization of a sequential epitope on the rabies virus glycoprotein which is recognized by a neutralizing monoclonal antibody, RG719. 857 83

We investigated unusual structures produced in BHK-21 cells infected with rabies virus (HEP-Flury strain). Sellers' staining of the cells revealed, in addition to Negri body-like structures (inclusion bodies), production of a fuchsin-stained cytoplasmic structure (FCPS) which encircled the nucleus. The frequency of the FCPS-forming cells increased as replication progressed. The FCPS was different from the inclusion body because the former contained the viral glycoprotein (G) and matrix protein (M2) antigens, while the latter contained nucleocapsid antigens. In the early phase of infection, we observed accumulation of viral envelope antigens in a cytoplasmic structure that was considered to be expanded rough endoplasmic reticulum (rER) because of its concomitant increase in BiP content. Time-course studies suggested that the envelope antigen-containing structure, which was not stained with basic fuchsin, translocated to the perinuclear region to form the FCPS. FCPS formation was dependent on incubation temperature and was decreased at 30 degrees C, while the development of virus-induced cytopathic effect (CPE) was delayed. When the incubation temperature was shifted up to 37 degrees C, FCPS formation was induced again and progression of CPE was accelerated in approximate proportion to the increasing number of FCPS-positive cells. From these studies, we conclude that viral G proteins gradually accumulate in the rER with M2 protein and the expanded rER converts eventually into the FCPS, which may be closely related to accelerated host cell death.
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PMID:Studies on unusual cytoplasmic structures which contain rabies virus envelope proteins. 881 Oct 13


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