Figure 1.

Host kinases and phosphatases are involved in prototypical PV formation. HeLa cells were infected for 24 h (A) or 48 h (B) with C. burnetii in the presence of p38 (SB-203580), PKC (GF 109203X), PRL1 (pentamidine), or PP2B (gossypol) inhibitors and visualized by phase contrast microscopy. Typical phase translucent PV are indicated by red arrows (B). p38 inhibitors dramatically enhanced PV development [(A) right panel, arrowheads] at early times post-infection while PKC, PRL1, and PP2B inhibitors prevented vacuole formation (B). Control = infected, untreated cells.