Multiple Phosphatidylinositol 3-Kinases Regulate Vaccinia Virus Morphogenesis
Figure 9
PI3K inhibitors disrupt vaccinia virus maturation.
A. BHK cells were infected with MVA for 17 hours plus or minus PI3K inhibitors. Untreated samples exhibit characteristic virion morphogenesis (4100x, Glut/KMnO4 fixative). A′:1) Crescents; 2) Immature virions; 3) Mature virion, IMV; A″: 4) IEV; 5) CEV; 6) EEV. B. In cells treated with 50 µM AS1, virions at the immature to IMV transition, but not at later stages, are evident (10,000x, Glut/OsO4 fixative). a) Replication center and crescents; b) Immature virion; c) Immature virion with nucleoid. C. In cells treated with 50 µM AS2, virions at the IMV wrapping step but not at later stages are evident (6800x, Glut/KMnO4 Fix). a') Immature virion; b') IMV. Note the lack of virions associated with the plasma membrane, characteristic of IEV inhibition. D. HeLa cells were infected with B5-GFP WR for 17 hours plus or minus PI3K inhibitors. Untreated samples exhibit characteristic virion morphogenesis (10,000x, Glut/KMnO4 Fix). D': 1) Crescents; 2) Immature virions; D″: 3) Mature virion, IMV; 4) IEV. E. In cells treated with 50 µM AS1, virions at the immature to IMV transition, but not at later stages, are evident (10,000x, Glut/OsO4 Fix). a) Viral crescents; b) Immature virion; c) Immature virion with nucleoid. F. Samples treated with 50 µM AS2 are stuck at the IMV wrapping step (7000x, Glut/KMn4). a′) Crescents; b′) Immature virion; c′) IMV. Note the lack of virions associated with the plasma membrane, a characteristic of IEV inhibition.