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. Author manuscript; available in PMC: 2019 Mar 1.
Published in final edited form as: Virology. 2018 Jul 26;522:244–259. doi: 10.1016/j.virol.2018.06.018

Fig. 1. Chimeric VSVΔG-CHIKV infects glioblastoma, melanoma, and breast cancer cells.

Fig. 1.

A. Schematic illustration (top) showing genomes of wild-type VSV and chimeric VSVΔG-CHIKV in which the VSV glycoprotein G gene (blue) has been replaced with the chikungunya glycoprotein sequence from the CHIKV structural polyprotein (pink). The diagram below illustrates this replacement in assembled viral particles. B. VSVΔG-CHIKV (MOI 0.02) was used to infect a collection of glioma cell lines from human (U373, U118, U87) and mouse (CT-2A) along with primary cultures of human glia and mouse glia. 3 days post infection (3 dpi), cells were visualized by immunolabeling with a primary antibody against VSV together with a secondary fluorescent antibody; cells were also stained with blue Hoechst33342 nuclear stain. Arrows indicate infected (red arrow) and uninfected (white arrow) cells. C. Infection of human melanoma (YUMAC, 501mel) and breast cancer (MDA-MB-436, MDA-MB-231, BT-549) cells 3 dpi. Scale bars 50 μm. D. VSVΔG-CHIKV (MOI 0.02) was used to test infection of human glioma cells (U373, U118, U87), mouse glioma (CT-2A), primary cultures of normal human glia and mouse glia, human melanoma (YUMAC, 501mel) and human breast cancer (MDA-MB-436, MDA-MB-231, BT-549) cells, 3 days post infection (3 dpi). Uninfected cells are identified with phase contrast microscopy. Statistical comparisons are between tumor cells and the normal human cells (glia). Values are reported as the mean ± SEM; n = 6. *p < 0.05, * *p < 0.01, * **p < 0.001 one-way ANOVA with repeated measures.