Abstract

Parasites of the genus Leishmania have the striking ability to survive in hydrolytic environments encountered throughout their digenetic life cycle. In one part of the life cycle, the parasite assumes an extracellular, flagellate promastigote form in the alimentary tract of its insect vector, the phlebotomine sandfly. Upon inoculation into a human or other suitable host, the parasite proliferates as an intracellular, nonflagellate amastigote in the phagolysosomes of phagocytic cells. Thus, to survive, the Leishmania must avoid destruction in (1) the sandfly gut where the parasite could be vulnerable to a variety of digestive enzymes, (2) the bloodstream of the host where the organism transiently exists and would be exposed to the lytic complement pathway, and, most spectacularly, (3) in the phagolysosome of host macrophages where the parasite would be subject to a number of hydrolytic enzymes and the microbicidal oxidative burst. Little is known about the molecular details of how this pathogen survives in obviously hostile environments. Cell surface glycoconjugates undoubtedly play a key role in the survival of the Leishmania parasite throughout its existence. The major cell surface glycoconjugate of the promastigote form is a polydisperse lipid-containing polysaccharide called lipophosphoglycan (LPG). Current information is reviewed that suggests that this interesting molecule is multifunctional.

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