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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spike glycoprotein (G protein) of rabies virus (CVS strain) expressed in HeLa cells from cloned cDNA mediated membrane fusion after exposure to pHs of 6.1 or below. Chemical crosslinking showed that the rabies G protein, like the vesicular stomatitis virus (VSV) G protein, could be crosslinked to dimers and trimers, indicating that rabies G protein is a trimer. However, unlike the VSV G protein, rabies G protein trimers were not stable to sedimentation in sucrose gradients, even at a mildly acidic pH which stabilizes the VSV G protein trimers. In addition, we report that the expressed rabies virus G protein was functional because it could assemble into VSV particles (tsO45) lacking VSV G protein and rescue infectivity. These VSV (rabies) pseudotypes were neutralized only by an antibody to the rabies G protein. We also examined the properties of a hybrid protein containing the extracellular domain of the rabies virus glycoprotein and the transmembrane and cytoplasmic domains of the VSV G protein. This protein was transported to the cell surface and could be crosslinked to form dimers and trimers, but had little or no detectable membrane fusion activity. The lack of fusion activity was paradoxical because the hybrid protein could rescue VSV infectivity, although the titers were lower than those obtained with the wild-type rabies G protein.
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PMID:Membrane fusion activity, oligomerization, and assembly of the rabies virus glycoprotein. 166 Feb

Acute infection of cloned BHK21 cells with rabies virus (CVS strain) resulted in a reduction in the amount of cellular RNA, not so rapid and pronounced as with another rhabdovirus, vesicular stomatitis virus (VSV). This decrease in the amount of cellular RNA was shown to be caused by a differential membrane permeability of infected and uninfected BHK21 cells to [3H]-uridine and by a real inhibition of cellular RNA synthesis.
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PMID:[Effects of rabies infection on the metabolism of the host-cell: does inhibition of cellular RNA synthesis take place?]. 258 78

We have determined the nucleotide sequence of the 3'region of the rabies genome (PV strain). This work is a first step in a project aimed at establishing the complete primary structure. From the 3'nucleotide sequence of the RNA genome, an octadecanucleotide complementary to the 3'extremity was constructed and used to prime cDNA synthesis. Two overlapping recombinant cDNA clones hybridizing with the nucleoprotein mRNA (NmRNA) were isolated and sequenced. The 1500 first nucleotides of the rabies genome cover two transcriptional units: the leader RNA and the NmRNA which was shown to be initiated around residue 59 by S1 nuclease protection experiments. Comparison between rabies PV and CVS strains up to residue 180 suggests a rapid evolution in the leader region. Studies of the sequence relationships between the 3'regions of two Rhabdoviruses, rabies virus and Vesicular Stomatitis Virus (VSV), demonstrate that there is a segmented homology. Stretches of highly conserved amino acids possibly involved in the interaction with the RNA genome were observed in the N protein, despite a wide divergence in the remaining sequence. In addition, the high homology between the transcription start and stop signals reflects the conservation of a similar transcriptional mechanism in these two non segmented negative strand RNA viruses.
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PMID:Primary structure of leader RNA and nucleoprotein genes of the rabies genome: segmented homology with VSV. 300 96

Resistance to superinfection with vesicular stomatitis virus (VSV) occurred in GL-V3 monkey kidney cells infected with the CVS-11, Pitman Moore, LEP Flury, but not the ERA strain of rabies virus. Specific immunofluorescent staining of intracellular rabies antigen showed that the number and size of fluorescent foci increased after the onset of interference, and that this was paralleled by increasing yields of infectious virus. Although CVS-11 and ERA differed in their ability to induce interference, the virus yields from monolayers infected with either strain were similar. Interference apparently had no effect on the replication or dissemination of the inducing virus, and seems unrelated to the long incubation period or aberrant forms of infection in vivo.
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PMID:Interference induced in GL-V3 monkey kidney cells by rabies virus strains. 626 82

We have isolated and characterized the RNA of intracellular virus nucleocapsids recovered from a number of cell cultures persistently infected with rabies virus or vesicular stomatitis virus (VSV). VSV persistent infections in BHK21, L cells and Aedes albopictus (mosquito) cells generally showed the presence of large amounts of defective-interfering (DI) nucleocapsid RNA and much smaller amounts of standard (B) nucleocapsid RNA. Persistent infections of BHK21 cells by two rabies virus strains, challenge virus standard (CVS-11) or HEP-Flury, were followed for several months during which time the ratio of DI to B nucleocapsid RNA cycled dramatically. We also observed coordinated fluctuations in the absolute amount of incorporation of [3H]uridine into virus nucleocapsid RNA. Total incorporation was generally highest following a decrease in the relative amount of DI nucleocapsid RNA synthesis. At no time were DI nucleocapsids absent in any of the persistently infected cultures.
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PMID:Analysis of viral and defective-interfering nucleocapsids in acute and persistent infection by rhabdoviruses. 628 69

The inhibiting activity of various human serum lipoprotein classes and their lipid components on the infectivity of rhabdoviruses has been studied. The research has been carried out according to different experimental procedures on both the vesicular stomatitis virus (Indiana strain), and the fixed rabies virus (CVS strain). The results obtained have shown an inhibition of the infectivity of VSV and CVS, mainly linked to the very low and low density lipoprotein classes. It has also been demonstrated that the inhibitors act directly on viruses causing a decrease in their attachment to host cells.
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PMID:Activity of human serum lipoproteins on the infectivity of rhabdoviruses. 630 4

The existence of specific rabies virus (RV) glycoprotein (G) binding sites on the surfaces of neuroblastoma cells is demonstrated. Spodoptera frugiperda (Sf21) cells expressing G of the RV strain CVS (Gcvs-Sf21 cells) bind specifically to neuroblastoma cells of different species but not to any other cell type (fibroblast, myoblast, epithelial, or glioma). Attachment to mouse neuroblastoma NG108-15 cells is abolished by previous treatment of Gcvs-Sf2 cells with anti-G antibody. Substitutions for lysine at position 330 and for arginine at position 333 in RV G greatly reduce interaction between Gcvs-Sf21 cells and NG108-15 cells. These data are consistent with in vivo results: an avirulent RV mutant bearing the same double mutation is not able to infect sensory neurons or motoneurons (P. Coulon, J.-P. Ternaux, A. Flamand, and C. Tuffereau, J. Virol. 72:273-278, 1998) after intramuscular inoculation into a mouse. Furthermore, infection of NG108-15 cells by RV but not by vesicular stomatitis virus leads to a reduction of the number of binding sites at the neuronal-cell surface. Our data strongly suggest that these specific attachment sites on neuroblastoma cells represent a neuronal receptor(s) used by RV to infect certain types of neurons in vivo.
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PMID:Neuronal cell surface molecules mediate specific binding to rabies virus glycoprotein expressed by a recombinant baculovirus on the surfaces of lepidopteran cells. 944 3

The contribution of rabies virus (RV) glycoprotein (G) in viral distribution in the brain was examined by immunohistochemistry following stereotaxic inoculation into the rat hippocampus. Viruses used in this study include the highly neuroinvasive challenge virus standard strains (CVS-N2C and CVS-B2C) and the nonneuroinvasive attenuated SN-10 strain, as well as SN-10-derived recombinant viruses expressing the G gene from CVS-N2C (RN2C) or CVS-B2C (RB2C). The distribution of recombinant viruses in the brain was similar to those of the parental viruses from which the G was derived. For example, while CVS-B2C- and RB2C-infected neurons were seen preferentially in the hippocampus, cortex, and hypothalamus, CVS-N2C- and RN2C-infected neurons were preferentially found in the hippocampus, cortex, and thalamus. SN-10 infected efficiently almost all the brain regions. To further study the role of the RV G in virus spreading, we examined the distribution of RV antigen in brains infected with a recombinant RV in which the SN-10 G was replaced with vesicular stomatitis virus (VSV) G (SN-10-VG) was examined. The spreading of SN-10-VG to the cortex and the thalamus was drastically reduced, but the number of infected neurons in hippocampus and hypothalamus, particularly the paraventricular nucleus, was similar to the SN-10 virus. This pattern of spreading resembles that of VSV. Together, our data demonstrate that it is the G protein that determines the distribution pattern of RV in the brain.
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PMID:The rabies virus glycoprotein determines the distribution of different rabies virus strains in the brain. 1216 19

The avian retroviruses reticuloendotheliosis virus strain A (REV-A) and spleen necrosis virus (SNV) are not naturally infectious in human cells. However, REV-A-derived viral vectors efficiently infect human cells when they are pseudotyped with envelope proteins displaying targeting ligands specific for human cell-surface receptors. Here we report that vectors containing the gag region of REV-A and pol of SNV can be pseudotyped with the envelope protein of vesicular stomatitis virus (VSV) and the glycoproteins of different rabies virus (RV) strains. Vectors pseudotyped with the envelope protein of the highly neurotropic RV strain CVS-N2c facilitated cell type-specific gene delivery into mouse and human neurons, but did not infect other human cell types. Moreover, when such vector particles were injected into the brain of newborn mice, only neuronal cells were infected in vivo. Cell-type-specific gene delivery into neurons may present quite specific gene therapy approaches for many degenerative diseases of the brain.
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PMID:Cell-type-specific gene delivery into neuronal cells in vitro and in vivo. 1451 61

Lentiviral vectors have proved an effective method to deliver transgenes into the brain; however, they are often hampered by a lack of spread from the site of injection. Modifying the viral envelope with a portion of a rabies envelope glycoprotein can enhance spread in the brain by using long-range axon projections to facilitate retrograde transport. In this study, we generated two chimeric envelopes containing the extra-virion and transmembrane domain of rabies SADB19 or CVS-N2c with the intra-virion domain of vesicular stomatitis virus. Viral particles were packaged containing a green fluorescent protein reporter construct under the control of the phosphoglycerokinase promoter. Both vectors produced high-titer particles with successful integration of the glycoproteins into the particle envelope and significant transduction of neurons in vitro. Injection of the SADB19 chimeric viral vector into the lumbar spinal cord of adult mice mediated a strong preference for gene transfer to local neurons and axonal terminals, with retrograde transport to neurons in the brainstem, hypothalamus and cerebral cortex. Development of this vector provides a useful means to reliably target select populations of neurons by retrograde targeting.
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PMID:Chimeric rabies SADB19-VSVg-pseudotyped lentiviral vectors mediate long-range retrograde transduction from the mouse spinal cord. 2563 Sep 49


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