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Hijacking the Cell : Minireview Parasites in the Driver ’ s Seat
| Content Provider | Semantic Scholar |
|---|---|
| Author | Beverley, Stephen M. |
| Copyright Year | 1996 |
| Abstract | brane fusion. Simultaneously, it sets about gaining acProtozoan parasites have evolved a remarkable ability cess to cellular nutrients by forming small pores in the to survive in their hosts, often for long periods of time vacuolar membrane (Schwab et al., 1994). In this manner and sometimes with minimal pathogenicity. The mechait enjoys a rich and comfortable life-style at the host nisms employed are as diverse as the evolutionary oricell's expense. gins of this group, which can be appreciated by examinEven more spectacular is the process conducted by ing any of the recently developed “trees of life” based malaria while entering the host's red blood cells, noron slowly-evolving molecules such as ribosomal RNAs mally completely lacking intracellular membrane traf(Sogin et al., 1989). Protozoan parasitesemerge from the ficking and endocytic pathways. Here, the parasite must most ancient eukaryotic lineages, with branches much force its way into the host cell, again with the aid of the deeper than those observed among the younger metaproducts of its apical organelles, but now creating a zoan kingdoms of fungi, plants, and animals. Reflecting parasitophorous vacuole completely de novo. Once intheir antiquity, the study of protozoans has yielded side, malaria then erects a new secretory pathway outabundant examples of molecular novelty, including new side of itself, leading from the parasite and its parasitoorganelles (hydrogenosomes in trichomonads, glycophorous vacuole, through the infected cell all the way somes and kinetoplast DNA networks in trypanosoto the erythrocyte surface, and complete with a variety matids, rhoptries and micronemes in apicomplexans) of membranous components undoubtedly involved in and molecular phenomena (bent DNA, glycosylphostrafficking (Haldar and Holder, 1993). Enzymes normally phatidyl inositol (GPI) protein anchors, trans-splicing, associated with the synthesis of the internal secretory RNA editing, programmed DNA rearrangements). Espepathway occur in the extracellular secretory pathway cially for the latter, their discovery in protozoa often as well, suggesting that it may be synthesized at least has led the way to appreciation of their importance in partially in situ (Elmendorf and Haldar, 1994). The extra“higher” creatures. cellular secretory pathway allows the parasite to radiMost parasitic lineagesderive from non-parasitic ancescally modify and reshape the host cell. Proteins such tors, and during the course of evolution each has solved as those encoded by the P. falciparum var gene family the survival puzzle in a different manner. Traditionally, are deposited on the erythrocyte surface, and mediate studies have focused upon how parasites resist host desequestration of infected cells in the peripheral vasculafenses, by antigenic variation, resistance to complement ture away from the protective clearing action of the and immunological attack, and/or escape to “safe” comspleen (Smith et al., 1995). This is a fantastic system in partments such as the host cell cytoplasm. What we are which the genesis of protein trafficking systems can be now learning is the extent to which intracellular parasites studied, and the use of the Green Fluorescent Protein have become masters at manipulating the structure and in transfected parasites (Ha et al., 1996; Figure 1 shows pathways of the host cell for their own nefarious purposes, an example for Leishmania) should facilitate this. The in order to create a more hospitable environment. One novelty of the extracellular pathway offers an attractive strategy commonly taken is a major remodeling of host target for those inevitably seeking to treat this dreaded cell compartments, thereby radically changing the cell's disease (Lauer et al., 1995). architecture and function. Another is a sophisticated maManipulation of Host Cell Signaling Pathways nipulation of host cell signaling pathways, inhibiting some Like Toxoplasma, the kinetoplastid protozoan Trypanoin order to preclude hostile responses or, even more resoma cruzi is able to invade a number of mammalian markably, activating others in order to exploit them for cell types. In doing so, the parasite must successfully invasion and/or survival. How the parasites accomplish interact with two different signaling systems. The first these feats is for the most part not well understood, and is the TGFb pathway, which is essential for parasite the emergence of genetic methods in these organisms invasion (Ming et al., 1995). The mechanism by which over the last few years promises an exciting future in this pathway contributes to survival is unknown, and it answering these questions. raises the possibility that T. cruzi possesses intrinsic Remodeling and/or Construction of TGFb activity of its own, the nature and origins of which Parasite-Friendly Compartments promise to be of great interest. Reliance upon TGFb- |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://beverleylab.wustl.edu/PDFs/088.%20%20Beverley%20Cell%201996.pdf |
| Alternate Webpage(s) | http://microbiology.wustl.edu/Bio_Sketches/beverleypub/088.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
