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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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Thermo Fisher live/dead viability kit reagent ( calcein am and ethidium homodimer-1 (ethd-1)
VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium <t>homodimer</t> <t>1</t> (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.
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Image Search Results


VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium homodimer 1 (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.

Journal: Virology

Article Title: Chikungunya-vesicular stomatitis chimeric virus targets and eliminates brain tumors

doi: 10.1016/j.virol.2018.06.018

Figure Lengend Snippet: VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC (MOI 1) were used to infect glioma cells derived from human (U118) and mouse (CT-2A). A,B. One day post-infection, cells were visualized by immunolabeling (green) with a primary antibody against VSV together with a secondary fluorescent antibody. C,D. Prior to immunolabeling, dead cells were labeled (red) using ethidium homodimer 1 (EthD). Bar graphs display mean percentage ± SEM of indicated cell counts; n = 6 and * **p < 0.001 one-way ANOVA with repeated measures. E. Diagram showing the relative size of viral plaques that developed 48 h post-infection on monolayer cultures of human (U118, U87) and mouse (CT-2A) glioma cells using VSVΔG-CHIKV, VSVwt and VSV-LASV-GPC. Each circle depicts the mean plaque size of 20 randomly selected plaques; the SEM is indicated by the black line projecting from each. Scale bar 0.55 mm. F. Bar graph shows mean plaque sizes in mm2 ± SEM; n = 20. **p < 0.01, ***p < 0.001, one way ANOVA with repeated measures.

Article Snippet: Finally, cells were incubated in nuclear stain Hoechst33342 (5 mg/ml in PBS) or, for cell death experiments, ethidium homodimer 1 (EthD-1; cat no. 40010; Biotium Inc, Fremont, CA) 2 μM in PBS for 20 min in the dark.

Techniques: Derivative Assay, Infection, Immunolabeling, Labeling