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  • 1
    Online Resource
    Online Resource
    Characterization of regulatory functions of the varicella-zoster virus gene 63-encoded protein
    American Society for Microbiology ; 1992
    In:  Journal of Virology Vol. 66, No. 6 ( 1992-06), p. 3899-3903
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 66, No. 6 ( 1992-06), p. 3899-3903
    Abstract: Varicella-zoster virus (VZV) gene 63 encodes a protein (IE63) with a predicted molecular mass of 30.5 kDa which has amino acid similarities to the immediate-early (IE) protein 22 (ICP22) of herpes simplex virus type 1. ICP22 is a polypeptide synthesized in herpes simplex virus type 1-infected cells, and as is the case for its VZV counterpart, its regulatory functions are unknown. On the basis of the VZV DNA sequence, it has been shown that IE63 exhibits hydrophilic and acidic properties, suggesting that this protein could play a regulatory role during the infectious cycle. We report in this article cotransfection experiments which demonstrate that the VZV gene 63 protein strongly represses, in a dose-dependent manner, the expression of VZV gene 62. On the other hand, transient expression of the VZV gene 63 protein can promote activation of the thymidine kinase gene but cannot affect the expression of the genes encoding glycoproteins I and II. The results of transient expression experiments strongly suggest that the VZV gene 63 protein could play a pivotal role in the repression of IE gene expression as well as in the activation of early gene expression.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.66.6.3899-3903.1992
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1992
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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  • 2
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    Online Resource
    Acute and persistent varicella‐zoster virus infection of human and murine neuroblastoma cell lines
    Wiley ; 1990
    In:  Journal of Neuroscience Research Vol. 26, No. 1 ( 1990-05), p. 90-97
    Details
    In: Journal of Neuroscience Research, Wiley, Vol. 26, No. 1 ( 1990-05), p. 90-97
    Abstract: Human and murine neuroblastoma cell lines were infected in vitro with varicella‐zoster virus (VZV). Infected human neuroblastoma cells (IMR‐32) supported the synthesis of abundant viral antigens as detected by indirect immunoperoxidase labeling using human serum rich in anti‐VZV antibodies and did not survive the infection. In situ hybridization (ISH) with VZV‐cloned probes revealed a strong hybridization signal in these infected cells. During cultivation, the virus was released in the culture medium, and viral polypeptides were revealed by Western blotting of infected cells, using either a monoclonal anti‐gpI antibody or a rabbit antiserum. All these findings indicate that IMR‐32 cells support a productive and lytic infection by VZV, whether infected by cell‐free virus or by cocultivation with infected cells. Murine neuroblastoma cells (neuro‐2A) survived VZV infection and did not produce any infectious virus. No VZV‐specific proteins were detected in infected cells either by immunolabeling or by Western blotting. However, viral nucleic acids could be detected by ISH, indicating that mouse neuroblastoma cells displayed a nonproductive, nonlytic infection. Infected neuro‐2A cells have been examined by ISH using probes corresponding to immediate early (IE) genes 4, 62, and 63 and late (L) gene 31 encoding gpII. A strong hybridization signal was detected when infected cells were probed with a fragment containing the IE genes 62 and 63. Lower levels of hybridization were detected with the other probes, corresponding to IE or L genes. These systems allow comparative molecular analysis of persistent and acute infection of nerve cells by VZV.
    Type of Medium: Online Resource
    ISSN: 0360-4012 , 1097-4547
    URL: Issue
    URL: Article
    DOI: 10.1002/jnr.v26:1
    DOI: 10.1002/jnr.490260111
    Language: English
    Publisher: Wiley
    Publication Date: 1990
    detail.hit.zdb_id: 1474904-X
    detail.hit.zdb_id: 195324-2
    SSG: 12
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  • 3
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    An in vivo model of varicella‐zoster virus latent infection of dorsal root ganglia
    Wiley ; 1990
    In:  Journal of Neuroscience Research Vol. 26, No. 1 ( 1990-05), p. 83-89
    Details
    In: Journal of Neuroscience Research, Wiley, Vol. 26, No. 1 ( 1990-05), p. 83-89
    Abstract: We describe here the first in vivo model of varicellazoster virus (VZV) latent infection in the adult rat peripheral nervous system. Infected Mewo cells were injected subcutaneously along the spine of healthy adult rats. No clinical sign of infection was observed even 9 months after inoculation. Humoral immune response to VZV was detected in all infected animals throughout the study (9 months). The presence of viral material in dissociated and cultured dorsal root ganglia (DRG) from inoculated animals was studied by immunoperoxidase and in situ hybridization. When DRGs from infected animals were plated in culture from 1 month and up to 9 months after inoculation, viral nucleic acids and proteins were detected in neurons. Furthermore, trypsinization and subcultivation of infected neurons in culture is needed to reactivate infectious virus at least in some of the neurons. This model provides a useful tool for studying (1) the molecular mechanisms leading to an in vivo latency, (2) the role of the immune system, in particular cellular immunity, on the establishment, maintenance, and reactivation of latency, (3) the neurotropism of mutant viruses, and (4) the effects of antiviral agents.
    Type of Medium: Online Resource
    ISSN: 0360-4012 , 1097-4547
    URL: Issue
    URL: Article
    DOI: 10.1002/jnr.v26:1
    DOI: 10.1002/jnr.490260110
    Language: English
    Publisher: Wiley
    Publication Date: 1990
    detail.hit.zdb_id: 1474904-X
    detail.hit.zdb_id: 195324-2
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Antibodies to varicella-zoster virus modulate antigen distribution but fail to induce viral persistence in vitro
    American Society for Microbiology ; 1992
    In:  Journal of Virology Vol. 66, No. 12 ( 1992-12), p. 7499-7504
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 66, No. 12 ( 1992-12), p. 7499-7504
    Abstract: Varicella-zoster virus (VZV) persists in human sensory ganglia. One of the hypotheses to explain the induction or the maintenance of VZV latency is that it could be promoted by the immune response itself. It is known that in the case of viruses which bud off the infected cell membrane, virus-specific antibodies can induce antigenic modulation, i.e., spatial redistribution of viral antigens and modulation of their synthesis. To determine whether antigenic modulation occurs during VZV infection in vitro and could possibly be involved in viral persistence, we have grown infected cells in the presence of anti-VZV antibodies either transiently or permanently. The distribution of immune complexes and viral proteins was then analyzed. In transient immunomodulation experiments, the distribution of one or more viral antigens was modified not only in the cytoplasmic membranes but also in the cytoplasm and nucleoplasm of infected cells. When infected cells were kept permanently in the presence of antibodies, the same pattern of redistribution of immune complexes was observed and the localization of internal viral glycoproteins was significantly modified. However, antibodies did not prevent the lytic effect of infection; they altered neither the infectious virus yield nor the Western immunoblot pattern of viral proteins, suggesting that immunomodulation is not the primary effector of viral persistence.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.66.12.7499-7504.1992
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1992
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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  • 5
    Online Resource
    Online Resource
    Characterization of the regulatory functions of varicella-zoster virus open reading frame 4 gene product
    American Society for Microbiology ; 1993
    In:  Journal of Virology Vol. 67, No. 7 ( 1993-07), p. 4379-4385
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 67, No. 7 ( 1993-07), p. 4379-4385
    Abstract: Varicella-zoster virus (VZV) open reading frame 4 (ORF4) encodes a protein with a predicted molecular weight of 51,540 presenting amino acid sequence homology with the immediate-early regulatory protein ICP27 of herpes simplex virus type 1. To investigate the regulatory properties of the ORF4 gene product, we performed a series of transient expression assays in Vero cells, using a plasmid expressing ORF4 as effector and several VZV genes and heterologous genes as targets. The VZV target plasmids contained promoter/regulatory regions from genes belonging to the three putative VZV kinetic classes fused to the chloramphenicol acetyltransferase (CAT) gene. The heterologous target plasmids consisted of promoter/regulatory regions of human cytomegalovirus, Rous sarcoma virus, and human immunodeficiency virus type 1 fused to the reporter gene. These experiments demonstrated that the ORF4 gene product activated expression of ORF62 in a dose-dependent fashion but had no effect on the expression of the three other putative immediate-early genes (ORF4, ORF61, and ORF63). When various amounts of ORF4 were transfected in the presence of early gene promoters, dose-dependent transactivation was evidenced with the thymidine kinase gene (ORF36) and the major DNA-binding protein gene (ORF29) promoters; interestingly, little activity was detected with the promoter of the DNA polymerase gene (ORF28). No activation of late gene expression, represented by the glycoprotein I and glycoprotein II genes, was seen even over a wide range of concentrations of input ORF4 plasmid. Expression of pCMVCAT, pRSVCAT, and pHIVCAT was also stimulated by the ORF4 gene product. CAT mRNA analysis showed that activation of VZV target promoters occurs at the transcriptional and/or posttranscriptional level.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.67.7.4379-4385.1993
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1993
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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  • 6
    Online Resource
    Online Resource
    Varicella-zoster virus infection of adult rat sensory neurons in vitro
    American Society for Microbiology ; 1989
    In:  Journal of Virology Vol. 63, No. 7 ( 1989-07), p. 3155-3160
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 63, No. 7 ( 1989-07), p. 3155-3160
    Abstract: We report here an in vitro model of neuronal infection by varicella-zoster virus (VZV). Such a model has been achieved by using dissociated adult rat dorsal root ganglia cells infected by cocultivation with VZV-infected MRC5 cells or with cell-free virus. Indirect VZV immunolabeling, in situ hybridization, and neuron-specific immunolabeling demonstrated that VZV infection occurred selectively in neurons. VZV-specific immunolabeling detected a few neurons 1 or 2 days postinfection but not later. Genome detection using cloned VZV DNA probes revealed a hybridization signal primarily with RNA. Within 1 to 6 days postinfection, a progressive increase of VZV-specific hybridization was observed in up to 50% of the neurons. RNAs corresponding to immediate-early, early, and late genes were found, and transcripts of immediate-early gene 63 were particularly abundant.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.63.7.3155-3160.1989
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1989
    detail.hit.zdb_id: 1495529-5
    detail.hit.zdb_id: 80174-4
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