Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific intracytoplasmic organelles, annulate lamellae and radial cisternae, have been studied in several human tumours. Annulate lamellae are observed in all cases of leiomyoma, leiomyosarcoma, rhabdomyosarcoma and malignant melanoma, whereas radial cisternae are only found in a case of leiomyosarcoma. Annulate lamellae are characterized by stacks of parallel arrayed long cisternae showing alternative arrangement of annuli and sacs. Some of these cisternae are connected directly with rough-surfaced endoplasmic reticulum and there is continuity with the lumen and membrane. Radial cisternae are mainly composed of two structures: numerous short cisternae, which are a variant of annulate lamellae, and numerous spherical particles derived from the cisternae. The cisternae are arranged parallel or radially around particles measuring up to 1100 A in diameter. These particles consisting of an amorphous high electron dense material without distinct limiting membrane are organized in groups and vary in number. There is no evidence of a direct relationship between these structures and viral infection.
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PMID:Fine structural study of annulate lamellae complexes in human tumors. 85 Oct 30

Infection of rhabdomyosarcoma (RD) cells by coxsackie B5 virus (CBV5) was non-cytopathic, although low titres of infectious virus were produced after 24 h post-infection. The extent of CBV5 replication in RD cells increased after sequential passage of the virus in these cells. The RD cells from the first cycle of CBV5 infection were recovered and maintained in culture for 3 months (equivalent to 21 passages) releasing infectious virus throughout this period; these cells were considered to be persistently infected with CBV5 and were designated piRD cells. Coxsackie virus antigen was demonstrated in a small proportion of piRD cells by immunofluorescence staining. High resolution two-dimensional polyacrylamide gel electrophoresis was used to analyse the intracellular proteins prepared from piRD cells, three proteins were detected which were absent in uninfected RD cells. These new proteins were similar in charge to virus proteins induced during CBV5 lytic infection of HEp-2 cells. Quantitative densitometry of 2-dimensional protein profiles of piRD and uninfected cells showed no significant disruption of RD cell protein synthesis by the persistent virus infection. Three cloned cell lines were recovered from piRD cells, none of which showed evidence of infectious virus or virus-induced protein synthesis suggesting that the parental cell line was a carrier culture for CBV5.
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PMID:Non-cytopathic infection of rhabdomyosarcoma cells by coxsackie B5 virus. 132 61

Serotype 5 coxsackie B virus (CBV5) can establish in vitro persistent infections in human rhabdomyosarcoma (RD) cells. This paper describes the characterisation of the virus released from the persistently infected RD cell line designated piRD-3673. Although infectious virus was released for 42 sequential passages of piRD-3673 cells, no gross virus-specific cytopathic effect was detected when the cells were examined by light microscopy. Two-dimensional polyacrylamide gel electrophoresis was used to compare the virus released from piRD-3673 cells with the CBV5 isolate (CBV-3673) used to initiate the persistent virus infection. Two of the virus intracellular proteins (apparent molecular weights 33,000 and 39,000, designated p33 and p39, respectively) increased in their net basic charge for the virus released from piRD-3673 cells compared to CBV-3673; a reduction in the apparent molecular weights of p33 and p39 was also observed. The charge alteration for both p33 and p39 was a two-stage process, the accumulative effect of which resulted in p33 increasing in pI from 6.14 to 6.53 and p39 increasing in pI from 6.29 to 6.63. The first mutation of p33 and p39 occurred between passages 7 and 10 of piRD-3673 cells and affected both the charge and apparent molecular weight of these two proteins. The second mutation at passage 15 of piRD-3673 cells caused only a change in the charge of p33 and p39. Two other virus proteins (p54 and p75) showed no evidence of mutation over the same passage history of piRD-3673 cells. The virus released from piRD-3673 cells also differed from CBV-3673 by two further criteria, a reduction in plaque-forming efficiency in HEp-2 cells and increased virus replication in RD cells. These data on virus evolution are discussed in relation to the maintenance of persistent CBV infections and the presence of naturally occurring CBV variants.
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PMID:Evolution of coxsackie B virus during in vitro persistent infection: detection of protein mutations using two-dimensional polyacrylamide gel electrophoresis. 838 3

Human coronaviruses are associated with acute respiratory and enteric disease in man as such their target cells are probably the epithelial cells lining the respiratory and enteric tract. Attachment of virus to specific receptors on the cell surface is a major determinant of virus tropism in pathogenesis (1). Recently, aminopeptidase-N was identified as a cell receptor for the 229e coronavirus (2). Cell receptor(s) for OC43 coronavirus have not been identified. However, it is of pathologic significance that OC43 virus shares DNA sequence homology with the two coronavirus isolates, SK and SD, from the brain of patients with multiple sclerosis (MS) (3). Probing MS and control brain with probes specific for human, murine, porcine and bovine coronavirus by in situ hybridization resulted in the detection of coronavirus RNA in 12 of 22 MS brain samples; five of which were positive with the OC43 probe (4). A study of virus-ligand interactions of OC43 with human rhabdomyosarcoma (RD) cells, which are highly susceptible to virus infection, was undertaken to identify possible cell receptors. The binding of virus collected from the supernatant of infected cells to cell proteins immobilized on nitrocellulose paper was used to screen for virus-ligand interactions. The next step was the identification or development of antibodies to each of the ligands, and to test their ability to blockade receptor activity by culturing infected cells in medium containing the ligand antibodies and measuring the effect on virus yield. The preliminary experiments reported here reveal an interesting observation of strong affinity of OC43 virus for the HLA class I antigen.
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PMID:HLA class I antigen serves as a receptor for human coronavirus OC43. 850 72

The vif gene of the human immunodeficiency virus (HIV-1) is required for productive virus infection of primary blood mononuclear cells (PBMCs) and macrophages in vitro. Replication of HIV-1 vif- mutants in T-lymphoid cell lines varies and is dependent on the cell line used for virus production. To further understand the role of Vif in HIV-1 infection, we constructed to vif deletion mutants from a molecular clone derived from an African patient (HIV-1Zr6). Cell-free Zr6 vif- virus pools made from transfected rhabdomyosarcoma (RD) cells do not replicate when added to cultures of stimulated PBMCs. However, vif mutants were able to spread from transfected RD cells to PBMCs if cell-to-cell contact was permitted. By Western blot analysis, viral structural proteins expressed after transfection of RD cells by wild-type or vif mutant proviruses were indistinguishable. However, binding of vif mutants to PBMCs or to purified CD4 and virus internalization were significantly reduced when compared with wild-type virus. The defects in cell-free infection, CD4 binding, and internalization were rescued by transcomplementation using a vif expression plasmid. Our results suggest a novel level at which the HIV-1 vif gene product acts to enhance cell-free infection and indicate that vif plays an important role in promoting HIV-1 binding and internalization. Combined with the previous reports of vif's effect at other steps in infection, this suggests that vif is a pleuripotent gene product that affects multiple stages of the infective process.
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PMID:Cell-free HIV-1Zr6 vif mutants are defective in binding to peripheral blood mononuclear cells and in internalization. 892 9

CXCR4 (also termed fusin, LESTR, or HUMSTR) is a member of the G-protein-coupled chemokine receptor family with seven membrane-spanning domains. CXCR4 acts as a coreceptor for syncytium-inducing human immunodeficiency virus type 1 (HIV-1) strains, conferring entry into CD4+ cells. We show here that a novel mouse monoclonal antibody (12G5) that recognizes CXCR4 blocked cell-to-cell fusion and cell free-virus infection of CXCR4+ CD4+ RD rhabdomyosarcoma cells by seven HIV-1 and HIV-2 strains that had various cell tropisms for different CD4+ human cell types. Yet the majority of the members of the same virus panel resisted 12G5 inhibition on T-cell lines. When inhibition was observed on these cell types, it was both cell type and virus strain dependent. In at least one situation, 12G5 failed to block LAI infection of cells expressing CXCR4 as the only available coreceptor. Our observations suggest that CXCR4 could be processed or presented differently depending on the cell type, allowing some strains to evade 12G5 inhibition. Alternatively, since several of the viruses could infect certain CXCR4- CD4+ cell lines, it is conceivable that alternative coreceptors are active, enabling individual HIV strains to choose between compatible coreceptors during entry into cells. Moreover, the strain dependency of 12G5 inhibition implies that the interaction of different HIVs with CXCR4 varies.
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PMID:Inhibition of human immunodeficiency virus fusion by a monoclonal antibody to a coreceptor (CXCR4) is both cell type and virus strain dependent. 899 2

In order to better understand cellular responses to viral infection at the transcriptional level, we employed differential display RT-PCR to analyze mRNAs from RD rhabdomyosarcoma cells following infection with a neurovirulent enterovirus 71 (EV71) strain, compared with mRNAs from uninfected cells. Of 250 expressed sequence tags (ESTs) isolated, sequenced, and identified, all were of cellular origin except 1 that was of viral origin. Of these, 156 were individual distinctive clones, comprising 45 mRNAs showing unaltered expression and 111 mRNAs exhibiting upregulation or downregulation. Of the 45 uniformly expressed mRNAs, 14 represented unknown genes. Of the 111 differentially expressed mRNAs, 63 did not match any known genes. Forty-eight of the 111 mRNAs modified by EV71 infection matched known genes, including those encoding components of cell cycle, cytoskeleton, and cell death mediators; protein degradation mediators; mitochondrial-related proteins; components of protein translation and modification; and cellular transport proteins. The altered expression profiles of representative genes were authenticated by semiquantitative RT-PCR and real-time RT-PCR. We also identified a novel alternatively spliced transcript of TRIP7 thyroid receptor interactor protein; the putative human homolog of murine mc7 mRNA predominantly expressed in the brain; and a novel mRNA similar to that encoding vacuolar protein 8 involved in protein targeting. These results underscore the applicability of the mRNA differential display technique for elucidating the expression profiles of known and even novel genes in response to cellular infection with pathogenic viruses.
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PMID:Differential display RT-PCR analysis of enterovirus-71-infected rhabdomyosarcoma cells reveals mRNA expression responses of multiple human genes with known and novel functions. 1203 73

Enterovirus 71 infection causes significant morbidity and mortality in children, yet there is no effective treatment. In this study, a protein-bound pigment, allophycocyanin purified from blue-green algae is first reported to exhibit anti-enterovirus 71 activity. Allophycocyanin neutralized the enterovirus 71-induced cytopathic effect in both human rhabdomyosarcoma cells and African green monkey kidney cells. The 50% inhibitory concentration of allophycocyanin for neutralizing the enterovirus 71-induced cytopathic effect was approximately 0.045 +/- 0.012 microM in green monkey kidney cells. The cytotoxic concentrations of allophycocyanin for rhabdomyosarcoma cells and African green monkey kidney cells were 1.653 +/- 0.003 microM and 1.521 +/- 0.012 microM, respectively. A plaque reduction assay showed that the concentrations of allophycocyanin for reducing plaque formation by 50% were approximately 0.056 +/- 0.007 microM and 0.101 +/- 0.032 microM, when allophycocyanin were added at the state of viral adsorption and post-adsorption, respectively. Antiviral activity was more efficient in cultures treated with allophycocyanin before viral infection compared with that in the cultures treated after infection. Allophycocyanin was also able to delay viral RNA synthesis in the infected cells and to abate the apoptotic process in enterovirus 71-infected rhabdomyosarcoma cells with evidence of characteristic DNA fragmentation, decreasing membrane damage and declining cell sub-G1 phase. It is concluded that allophycocyanin possesses antiviral activity and has a potential for development as an anti-enterovirus 71 agent.
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PMID:Inhibition of enterovirus 71-induced apoptosis by allophycocyanin isolated from a blue-green alga Spirulina platensis. 1262 52

In several cell types, poliovirus activates the apoptotic program, implementation of which is suppressed by viral antiapoptotic functions. In such cells, productive infection leads to a necrotic cytopathic effect (CPE), while abortive reproduction, associated with inadequate viral antiapoptotic functions, results in apoptosis. Here, we describe two other types of cell response to poliovirus infection. Murine L20B cells expressing human poliovirus receptor responded to the infection by both CPE and apoptosis concurrently. Interruption of productive infection decreased rather than increased the proportion of apoptotic cells. Productive infection was accompanied by the early efflux of cytochrome c from the mitochondria in a proportion of cells and by activation of DEVD-specific caspases. Inactivation of caspase-9 resulted in a marked, but incomplete, prevention of the apoptotic response of these cells to viral infection. Thus, the poliovirus-triggered apoptotic program in L20B cells was not completely suppressed by the viral antiapoptotic functions. In contrast, human rhabdomyosarcoma RD cells did not develop appreciable apoptosis during productive or abortive infection, exhibiting inefficient efflux of cytochrome c from mitochondria and no marked activation of DEVD-specific caspases. The cells were also refractory to several nonviral apoptosis inducers. Nevertheless, typical caspase-dependent signs of apoptosis in a proportion of RD cells were observed after cessation of viral reproduction. Such "late" apoptosis was also observed in productively infected HeLa cells. In addition, a tiny proportion of all studied cells were TUNEL positive even in the presence of a caspase inhibitor. Degradation of DNA in such cells appeared to be a postmortem phenomenon. Biological relevance of variable host responses to viral infection is discussed.
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PMID:Variability in apoptotic response to poliovirus infection. 1562 72

Novel methods of local control for sarcomas are needed. We investigated the antitumor effect of two related herpes simplex virus (HSV) mutants, NV1020 and NV1066, on human rhabdomyosracoma cells and xenografts. Cell death correlated with virus replication and apoptosis in cultured cells and tumors. Complete regression was seen in all tumors <250 mm(3) following a single injection, yet only half of tumors >250 mm(3) showed a complete response. Fractionation of the virus dose into five injection sites did not increase transduction efficiency, transgene expression, or virus production, but did yield more widespread intratumoral distribution. Despite the same total dose of virus, improved control of large tumors was seen using fractionated injections as all large tumors (500-700 mm(3)) had durable, complete regression. Our data suggest that oncolytic HSVs may be useful for local control of bulky rhabdomyosarcoma tumors and that fractionated virus administration results in a more widespread virus infection and better tumor control. Therefore, strategies to maximize intratumoral virus distribution at initial delivery should be sought.
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PMID:Widespread intratumoral virus distribution with fractionated injection enables local control of large human rhabdomyosarcoma xenografts by oncolytic herpes simplex viruses. 1566 22


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