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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Virology. 2011 Jul 13;417(2):293–303. doi: 10.1016/j.virol.2011.06.010

Fig. 2. Viral replication in WT and −/− cells.

Fig. 2

A) i. The indicated BMK cell lines were infected with VSV (moi=0.001 or 0.0001) for 16 h, the conditioned medium was harvested and applied to indicator HT1080 cells in Log10 dilutions. After an additional 16–24 h, indicator cells were fixed and stained with crystal violet and viral titers quantified as the dilution providing 50% cytopathicity, and expressed as a value relative to that observed in WT BMK infected with moi=0.001. ii. To assess viral RNA accumulation, cells were infected with VSV (moi=0.001) for 0–96 h and then total cellular RNA was isolated and reverse transcribed into cDNA that was used as a template for RT-PCR analysis of VSV G-protein mRNA expression. GAPDH served as a cellular RNA control. B) WT BMK cells were infected with VSV (moi=0.001) for 16 h and then fixed and stained for immunofluorescent detection of VSV using a G-protein primary antibody and a FITC-conjugated goat anti-mouse secondary antibody. Cellular morphology was assessed by phase contrast microscopy, and cell nuclei were detected by DAPI staining. C) Noxa −/− BMK were infected with VSV for 16h or 96 h and then fixed and stained as in “B”.

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