(A) Reorganization of the host mitochondria (M), endoplasmic reticulum (ER), lysosomes, microtubules (MT), microtubule organazing center (MTOC) and intermediate filaments (IF) around the parasitophorous vacuole (PV). Acquisition of cholesterol (C) via the endocytosis of low density lipoproteins (LDL). Localization of the rhoptry proteins ROP16 and PPC2-hn in the host nucleus (hn) of the host cell soon after invasion. Phosphorylation of the transcriptions factors STAT3 and STAT6 in host cells infected with parasite of type I or III. Golgi apparatus (Go).
(B) Proteins of the parasitophorous vacuole membrane (PVM) ROP1,2,4,5,7,18 and GRA3,5,7,8,10. ROP2 is involved in the recruitment of mitochondria at the PVM. ROP14 is candidate to compose the PVM pore. PVM invaginations allow encroachment of lysosomes into the PV. MT and GRA7 are involved in the rearrangement of the PVM in a structure termed H.O.S.T. GRA2,3,4,6,9 are inserted in the intravacuolar network (IVN). GRA3,5,7,8 are associated with the parasitophrous vacuole extension (PVE).

T. gondii influences the apoptotic pathways of the host cell. The inactivation of the initiator caspases 8 and 9, as well as executioner caspases 3 and 7, is seen following invasion by T. gondii. Induction of apoptosis in host cell types I and II, via the tumor necrosis factor receptor (TNFR) and Fas death receptors, is inhibited by T. gondii through degradation of the caspase 8. Infection with T. gondii retards the release of the cytochrome c from the host mitochondria intermembrane space. The role of the host mitochondria and PVM association in the blockade of apoptosis is still unclear. Proteins released from the secretory organelles during invasion could be involved in the inhibition of executioner caspases 3 and 7. In certain cells, the transcription factor NF-κB translocates to the nucleus after infection where it promotes the expression of inhibitor of apoptotic proteins (IAP) and anti-apoptotic Bcl2-family proteins. The phosphorylation of the inhibitor κBα (IκBα) by host and parasite IKK proteins is involved in the activation of NFκB. Activation of the phosphoinositol 3 kinase (PI3K) pathway in infected cells leads to inactivation of the pro-apoptotic factor Bad, the inhibition of the transcription factor forkhead transcription factor (FKHR1) and to activation of the NF-κB pathway.