Characterization of the regulatory functions of varicella-zoster virus open reading frame-4 gene-product

in Journal of Virology (1993), 67(7), 4379-4385

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 ... [more ▼]

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. [less ▲]

Isolation And Characterization Of A 2.3-Kilobase-Pair Cdna Fragment Encoding The Binding Domain Of The Bovine Leukemia-Virus Cell-Receptor

in Journal of Virology (1993), 67(2),

Bovine leukemia virus, an animal model for the study of intrastrain variability.

in Journal of Virology (1993), 67(2),

A Cyclic Amp-Responsive Dna-Binding Protein (Creb2) Is A Cellular Transactivator Of The Bovine Leukemia-Virus Long Terminal Repeat

in Journal of Virology (1992), 66(2),

Antibodies to varicella-zoster virus modulate antigen distribution but fail to induce viral persistence in vitro.

in Journal of Virology (1992), 66(12), 7499-504

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 ... [more ▼]

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. [less ▲]

Varicella-zoster virus infection of adult rat sensory neurons in vitro.

in Journal of Virology (1989), 63(7), 3155-60

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 ... [more ▼]

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. [less ▲]

Chromosome Integration Domain for Bovine Leukemia Provirus in Tumors

in Journal of Virology (1983), 47(1), 146-150

Cloned Human Polyomavirus JC Can Transform Human Amnion Cells

in Journal of Virology (1980), 36

The genome of the human polyomavirus JC (Mad-1 strain) was molecularly cloned in Escherichia coli by using the plasmid vector pBR322. Recombinant DNA molecules were constructed with the entire JC genome ... [more ▼]

The genome of the human polyomavirus JC (Mad-1 strain) was molecularly cloned in Escherichia coli by using the plasmid vector pBR322. Recombinant DNA molecules were constructed with the entire JC genome inserted either at its unique EcoRI site at 0.0 map units or at its unique BamHI site at 0.51 map units. Viral DNA from each of these recombinant plasmids was capable of transforming human amnion cells, and cell lines established from transformed foci were positive for JC tumor antigen as assayed by indirect immunofluorescence. [less ▲]

Electron microscopic study of measles virus infection: cell fusion and hemadsorption

in Journal of Virology (1978), 28(2), 567-577

Virus-induced cell fusion has been studied after infection of Vero cells with measles virus. Scanning and transmission electron microscopy were combined with immunoperoxidase labeling of measles antigens ... [more ▼]

Virus-induced cell fusion has been studied after infection of Vero cells with measles virus. Scanning and transmission electron microscopy were combined with immunoperoxidase labeling of measles antigens to correlate viral production and distribution of virus-induced erythrocyte binding sites with progress of fusion-Release of infectious virus started before syncytia were detected and decreased while the number and size of syncytia were increasing. Most virions were seen budding from mononucleated cells or from the periphery of syncytia where cells were being recruited. Moving inward, the surfaces of syncytia were covered with numerous ridges containing viral antigen, but few viral buds were seen, suggesting that syncytia might be sites of defective viral formation. Hemadsorption occurred predominantly within the confines of syncytia. Erythrocytes were scattered sparsely over immature syncytia but were densely packed in the center of mature syncytia. Active binding sites for erythrocytes were located on cell villi and ridges covered with measles antigens. Hemadsorption was completely inhibited in measles virus-infected cultures pretreated with virus- specific immunoglobulin G for 1 h at 4°C. However, when these cultures were shifted to 37°C, hemadsorbing sites were recovered at the periphery of enlarging syncytia. Virus-induced sites for erythrocyte adsorption were found to move centripetally on syncytium membranes as fusion progressed. [less ▲]