Cell-fusion assay for the detection of rubella virus in Vero cells

Grutadauria, Sergio; Córdoba, Patricia; Cuffini, Cecilia; Zapata, Marta

doi:10.1016/s0928-0197(98)00019-1

Cited by 4 publications

(2 citation statements)

References 23 publications

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“…Gilchrist strain (GIL), prototype of laboratory, and Cordoba strain (COR), isolated at Cordoba, Argentina, of RV were used. Inoculums were titrated in Vero cells by the acid shock method, based on the capacity of RV proteins to induce syncytia formation (1,16). Viral titer is expressed in syncytia forming units per mL (SFU/mL) and multiplicity of infection (moi), in SFU per cell (SFU/cell).…”

Section: Methodsmentioning

confidence: 99%

Rubella Virus Does Not Induce Apoptosis in Primary Human Embryo Fibroblast Cultures: A Possible Way of Viral Persistence in Congenital Infection

et al. 2004

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Congenital rubella is a persistent infection that contrasts with acute postnatal infection. Basis of the Rubella virus (RV) persistence still remain unknown, though several hypotheses have been postulated. RV induces apoptosis in cell lines, maybe as a way of cell-autonomous defense mechanism against virus. Considering the pattern of c-oncogenes expression during embryogenesis, which promotes proliferation while it inhibits apoptosis in specific cells, at certain times, it can be proposed that when RV infection establishes early in gestation, embryo cells that are proliferating have their apoptotic pathways shut down; then infected proliferating embryo cells cannot execute their apoptotic death program. We here report that RV induces apoptosis in human normal-term placenta chorionic villi explants (CVE) and in monolayers of cytotrophoblasts (CTB), but does not induce apoptosis in primary human embryo fibroblasts (HEF) cultures. These results suggest distinct responses to RV infection when comparing differentiated cells, as CTB, to cells with high proliferating potential, as HEF. RV shoots apoptosis in the former, whereas in fibroblastic dividing cells derived from embryo, RV appears not to be enough stimulus to activate the genetic program of cell death.

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Section: Methodsmentioning

confidence: 99%

Rubella Virus Does Not Induce Apoptosis in Primary Human Embryo Fibroblast Cultures: A Possible Way of Viral Persistence in Congenital Infection

et al. 2004

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“…It is also an essential step for intercellular informational transmission. It has been reported that the spike proteins of RV can induce membrane fusion after being treated with fusion medium at low pH [11,12] . The mechanism of low-pH-induced membrane fusion is not completely understood, although it has been reported that low pH leads to irreversible conformational changes on the envelope proteins of some enveloped viruses [13] .…”

Section: Introductionmentioning

confidence: 99%

Effects of E2 and E1 Glycosylation on Specific Membrane Fusion in Rubella Virus Strain JR23

Liu

Wang

2009

Intervirology

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Objectives: To explore the effects of glycosylation in glycoprotein on membrane fusion in rubella virus strain JR23. Methods: The N-linked glycosylation sites in glycoproteins were mutated individually or in combination. Total expression and cell surface expression efficiencies of mutant proteins were assayed with Western blot and FACS. The fusion functions were assayed with Giemsa staining and reporter gene method. Binding activity of mutant proteins was detected with hemadsorption assays. Results: We observed that total expression levels of all the mutant proteins in cells were unchanged, but the cell surface expression efficiencies of all the mutant proteins except E2 S131V were lower than wild-type protein. When effects of reduced cell surface expression were eliminated, mutant proteins N53G, S73I, S131V and T78A had lower fusion activities than wild-type protein, and binding abilities of E2 S73I and E1 T78A decreased slightly. But in all the combined mutants, no cell fusion was detected, and only a minor hemadsorption was observed in N53G-S131V, N53G-T78A and N53G-T211A. Conclusions: Glycosylation of glycoproteins were involved in cell surface expression synergistically. Glycosylation on E2 N53, N71, N129 and E1 N76 altered the specific membrane fusion, whereas no effects were detected on E1 N177 and N209 individually.

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Apoptosis induction by the infection with Gilchrist strain of rubella virus

Martı́nez

Zapata

2002

Journal of Clinical Virology

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Cell-fusion assay for the detection of rubella virus in Vero cells

Cited by 4 publications

References 23 publications

Rubella Virus Does Not Induce Apoptosis in Primary Human Embryo Fibroblast Cultures: A Possible Way of Viral Persistence in Congenital Infection

Rubella Virus Does Not Induce Apoptosis in Primary Human Embryo Fibroblast Cultures: A Possible Way of Viral Persistence in Congenital Infection

Effects of E2 and E1 Glycosylation on Specific Membrane Fusion in Rubella Virus Strain JR23

Apoptosis induction by the infection with Gilchrist strain of rubella virus

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