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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth of two measles virus strains, the TYCSA and CAM, was compared in three continuous cell lines derived from the nervous tissues, human neuroblastoma IMR-32, human glioma 118MGC, and rat glioma C-6. The two human neural cells were shown to support the growth of both measles virus strains as efficiently as in the non-neural Vero cells. Different types of cytopathic effect (CPE) between the two virus strains were noticed in IMR-32 cells; the CAM strain induced strand-forming type CPE and the TYCSA strain giant-cell type CPE. As a difference of growth pattern between IMR-32 and 118MGC cells, virus antigen was demonstrated in both the nucleus and cytoplasm of 118MGC cells whereas virus antigen was present only in the cytoplasm of IMR-32 cells. In contrast to the productive infection in human neural cells, growth of both virus strains was restricted in rat glioma C-6 cells without showing CPE although the prolonged presence of virus antigens was demonstrated by the immunofluorescent technique.
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PMID:Growth of measles virus in continuous cell lines derived from the nervous tissues of human and rat. 51 97

The interaction of measles virus with RG-6 cells derived from rat glioma was investigated. When a culture of RG-6 cells was infected with measles virus, the synthesis of viral antigens was detected in very few cells, at most 5%. The apparent resistance to measles virus infection was also repeatedly found in all of the subclonal cells derived form RG-6 cells. Although all of the virus-synthesizing cells had the ability to form plaques on Vero cells, they produced only a reduced amount of infectious virus, i.e., 0.1 plaque-forming units per cell. These results imply the existence of some mechanism that regulates growth of measles virus in cultures of RG-6 cells. The transmission of genetic material of measles virus from infected RG-6 cells to Vero cells was not inhibited in the presence of antiviral serum. This fact may provide a basis for interpretation of the persistence of virus, in the presence of antibody, in patients with subacute sclerosing panencephalitis.
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PMID:Growth of measles virus in cultures of rat glioma cells. 80 59

Application of neutralizing anti-hemagglutinin antibodies to mouse neuroblastoma cells (NS20Y/MS) persistently infected with measles virus (MV) leads to a significant reduction of viral structural proteins within 6 days. While the transcriptional gradient for MV-specific mRNAs remained unaffected upon antibody treatment, the total amount of MV-specific transcripts dropped by 80% after 24 h. The expression of genomic RNA was affected similarly, with slightly slower time kinetics. Both transcription and expression of the viral structural proteins could be completely reactivated when viral antibodies were removed from the tissue culture. The same findings could be obtained in rat glioma cells persistently infected with subacute sclerosing panencephalitis virus (C6/SSPE) but not in cells of nonneural origin. The data indicate that antibody-induced antigenic modulation affects the early stages of viral transcription within a few hours after the addition of antibodies and leads to an almost complete repression of viral gene expression in cells of neural origin.
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PMID:Antibody-dependent transcriptional regulation of measles virus in persistently infected neural cells. 150 Dec 88

Endothelin 1 causes a strong Ca2+ signal in C6 rat glioma cells as measured by fura-2 fluorescence. This endothelin 1-induced Ca2+ signal was not observed when the cells were persistently infected with a measles virus strain of subacute sclerosing panencephalitis (SSPE, strain Lec). Binding of 125I-labeled endothelin 1 to the C6/SSPE cells was less than 5% of the binding to the C6 control cells, suggesting that the impairment in signal transduction was due to a loss of binding sites for endothelin 1. Treatment of the C6/SSPE cells with measles antiserum resulted in the loss of expression of viral proteins located in the membrane as well as inside the cells (antigenic modulation), but it restored neither the endothelin 1-induced Ca2+ rise nor the 125I-endothelin 1 binding. Cocultivation of uninfected C6 cells with C6/SSPE cells (9:1 ratio) resulting in contact-mediated transmission of measles virus showed that the 125I-endothelin 1 binding activity was gradually lost as a consequence of persistent virus infection.
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PMID:Loss of the endothelin signal pathway in C6 rat glioma cells persistently infected with measles virus. 165 Apr 80

Rat glioma C6 cells persistently infected with measles subacute sclerosing panencephalitis (SSPE) virus (C6/SSPE) express the viral membrane proteins haemagglutinin (HA) and F on their cell surface as well as the intracellular proteins N, P and M. Previously we have shown that the addition of a polyclonal antibody against the HA antigen to the growth medium of C6/SSPE cells led to a gradual loss of all viral antigens. Here we show that the addition of a monoclonal antibody (MAb K83) leads only to a transient decrease in viral antigens during the first three passages. After the third passage viral antigens start to increase and after five passages they produce more antigens than at the premodulation level. At this point of the MAb treatment, MAb K83 no longer recognized the HA antigen on the surface of the cells and in virus particles produced by these cells in contrast with polyclonal antibodies or other MAbs against the HA antigen. The results suggest that specific variants of the SSPE virus with an altered HA antigen were selected by the MAb treatment.
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PMID:Antigenic modulation of measles subacute sclerosing panencephalitis virus in a persistently infected rat glioma cell line by monoclonal anti-haemagglutinin antibodies. 169 67

C6 rat glioma cells persistently infected with subacute sclerosing panencephalitis virus (C6/SSPE) were treated with measles antiserum and purified anti-measles IgG. This stimulated phosphoinositide breakdown and an increase in inositol phosphates. In uninfected C6 cells, however, only fetal calf serum (FCS), but not measles antiserum could induce inositol polyphosphate production.
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PMID:Coupling of viral membrane proteins to phosphatidylinositide signalling system. 254 Oct 10

A monocyte chemotactic activity was found to be released by various types of cultured human cells after appropriate stimulation: normal diploid fibroblasts, peripheral blood mononuclear cells or monocytes isolated therefrom, and a number of tumor cell lines, including osteosarcoma (MG-63) and hepatoma (Malavu) but not melanoma (Bowes) cells. Cultures of diploid human fibroblasts and these tumor cells stimulated with interleukin (IL) 1 or double-stranded RNA [poly(rI).poly(rC)], or infected with viruses (measles or rubella viruses) were found to produce chemotactic activity for both monocytes and granulocytes. Media collected from fibroblasts treated with E. coli or IL 6 did not contain such activity. Granulocyte and monocyte chemotactic activities were serologically distinct, and could be separated by successive chromatographical procedures. While the granulocyte chemotactic activity of both fibroblasts and MG-63 cells had previously been identified as granulocyte chemotactic protein/IL 8, the monocyte chemotactic activity from MG-63 cells was identified by amino acid sequence analysis as a different protein recently described to be released by human glioma and myelomonocytic cell lines. In view of the similarity in their chromatographical behavior, monocyte chemotactic activities from fibroblasts, MG-63 cells and fresh monocytes can probably be assigned to identical molecules. Cultures of unfractionated peripheral blood cells, however, were found to release an additional monocyte chemotactic protein, identifiable by amino acid sequence analysis as platelet factor 4.
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PMID:Identification by sequence analysis of chemotactic factors for monocytes produced by normal and transformed cells stimulated with virus, double-stranded RNA or cytokine. 269 Dec 59

Cultivation of measles virus (SSPE virus, Lec strain) persistently infected C6 rat glioma cells at 39 degrees C resulted in the loss of detectable expression of measles virus proteins. Temperature shift-back led to reactivation of measles virus even after maintenance of the cells at 39 degrees C for 15 days. In Northern blot analysis viral mRNA disappeared at 3 days after shift-up whereas 50 S viral genome-sized RNA was detectable until 6 days. The 50 S RNA decreased in quantity in rough correlation with dilution by cell passage at 39 degrees C. The 50 S viral RNA was found in the nucleocapsid fraction. On day 9 after shift-down of persistently infected cells, maintained at 39 degrees C for 15 days, 50 S viral RNA reappeared although mRNAs were not yet detected. Infectious center assays showed that the number of cells in the population at 39 degrees C, which contained an SSPE virus genome that could be reactivated, declined after temperature shift. Moreover, cell cloning experiments, in which single cells of cultures maintained for various lengths of time at 39 degrees C were incubated at 35 degrees C and examined by immunofluorescence, reconfirmed the above results. This indicates that the reactivation of SSPE virus described here was due to re-infection of virus-antigen negative cells with progeny virus produced by a few latently infected cells in the population. The biological significance of this phenomenon in the central nervous system virus infection is discussed.
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PMID:Long-term effect of elevated temperatures on SSPE virus expression in persistently infected rat glial cells. 270 78

Rat glioma cells (C6) persistently infected with measles virus show a locally dissociated distribution of budding processes at the cell surface.
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PMID:Morphogenesis of measles virus on C6 rat glioma cells. 319 42

Maintenance of measles (SSPE-Lec) virus persistently infected C6 rat glioma cells in medium containing polyclonal measles antiserum resulted in the loss of detectable expression of all measles virus proteins. Removal of these cells from antiserum, however, led to a re-expression of virus proteins and the production of infectious virus. Cloning of antibody-modulated non-expressing cells in the presence of antiserum showed that re-expression of virus proteins was not due to an incomplete curing process following the addition of antiserum, as a large number of non-expressing cell clones developed the capacity to express measles virus antigen at different periods after removal of antiserum. Irradiation of persistently infected cells to give a non-growing culture showed that modulation was not mediated by a selection and outgrowth of a small percentage of non-expressing cells originally present in the culture. Antibody directed against C6 membrane proteins did not lead to modulation and it was also shown that only monoclonal antibodies with neutralizing activity could affect intracellular antigen expression. Immunoglobulin Fab fragments with neutralizing activity also had modulating activity. Although all modulated cell clones were more susceptible to homologous virus infection than control C6 cells, it was not possible to rescue any defective measles virus which may have been maintained in the culture.
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PMID:Effect of measles virus antibodies on a measles SSPE virus persistently infected C6 rat glioma cell line. 402 Mar 46


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