Redirection of host vesicle trafficking pathways by intracellular parasites.
Bacterial and protozoon intracellular parasites have evolved diverse mechanisms for evasion of host cellular defenses associated with adaptations for survival in distinct intracellular compartments. As the reagents identifying discrete steps in vesicle maturation and trafficking have become increasingly available, it has become clear that the vacuoles occupied by intracellular parasites are much more diverse than had been previously appreciated. Many parasites induce selective fusion competence with the vacuoles they occupy, without affecting vesicular trafficking elsewhere in the cell. A likely means of controlling vesicular interactions is modification of the parasitophorous vacuole membrane by the insertion of parasite-specific proteins. A rapidly expanding class of bacterial proteins that modify the vacuolar membrane are the chlamydial inclusion membrane proteins. Although the functions of most of these proteins remain to be defined, the majority are expressed early in the infectious process, suggesting that modification of the vacuole is critical to the outcome of the host-parasite interaction.
Hackstadt
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T
Host-Parasite Interactions Section, Laboratory of Intracellular Parasites, NIAID, Rocky Mountain Laboratories, Hamilton, MT 59840, USA. ted_hackstadt@nih.gov
D000818:Animals; D002689:Chlamydia / Q000472:pathogenicity* / Q000502:physiology*; D004705:Endocytosis; D010271:Parasites / Q000472:pathogenicity* / Q000502:physiology*; D010588:Phagosomes / Q000378:metabolism; D022161:Transport Vesicles / Q000378:metabolism*; D014617:Vacuoles / Q000378:metabolism