A hallmark of apicomplexan pathogens such as Plasmodium, Toxoplasma and Cryptosporidium is that they invade, replicate within, and then egress from their host cells. Egress usually results in lysis of the host cell, with deleterious consequences for the host. In the case of malaria, for example, much of the disease pathology is associated with cyclical waves of host erythrocyte destruction. This review highlights recent advances in mapping the signaling pathways that lead to egress and the parasite molecules involved in responding to and transmitting those signals. The review also discusses new findings for effector molecules that mediate disruption of the bounding membranes that enclose the intracellular parasite and the manner in which membrane rupture occurs to finally release invasive forms of the parasite.
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