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The phosphatidylinositol-3-phosphate 5-kinase inhibitor apilimod blocks filoviral entry and infection

Fig 3

Apilimod inhibits VLP entry and trVLP infection with similar potency.

(A) HEK 293T/17 cells were pretreated with the indicated concentration of apilimod or DMSO (0 μM) for 1 h at 37°C. VLPs were bound to the cells by spinfection in the presence of the indicated concentration of apilimod or DMSO. After incubation at 37°C (3 h), VLP entry was assayed. To assess cell viability, parallel 293T/17 cells were treated as for entry, but without VLPs or CCF2 loading. After 3 h at 37°C, cell viability was determined. (B) Cells (HEK 293T/17) pretreated as in (A) were infected with trVLPs (in the presence of the indicated concentration of apilimod) for 48 h at 37°C and infection by trVLPs was then assayed. To measure cell viability, parallel HEK 293T/17 cells were pretreated as above and then mock infected (± the indicated concentration of apilimod) for 48 h at 37°C followed by determination of cell viability. Antiviral activity is shown in blue and cytotoxicity is shown in red. (C) Comparison of normalized VLP entry (blue bars) and trVLP infection (red bars) inhibition; data are from (A) and (B). Data are averages of triplicate samples ± SD. Similar results for parallel tests of VLP entry and trVLP inhibition were observed in two additional experiments. Cell viability was tested in one of these experiments, and similar results were obtained. (D) BSC-1 cells were treated with apilimod and VLP entry was assayed as in (A). Data are averages of triplicate samples ± SD. Similar results were observed in an additional experiment.

Fig 3

doi: https://doi.org/10.1371/journal.pntd.0005540.g003