Host Cell Invasion

General Information

When a parasite comes into contact with a potential host cell, two series of events may occur which lead to intracellular parasitism. First comes a recognition step which enables a suitable close association between both partners, then comes the internalization of the organism within the host cell. The mechanisms of recognition are far from being entirely elucidated, as well as the ones by which entry occurs. Data have been obtained however, which show that the different parasite groups have evolved different strategies toward these goals.

A major question when dealing with host cell invasion by a pathogen is to decide whether this one actively enters a cell or whether it is engulfed by the process called phagocytosis. The matter is rather clear with those parasites which force their way through the plasma membrane of the host cell or fuse their membrane with it; it is more confusing when internalization occurs within a parasitophorous vacuole, the membrane of which is continuous with the host cell plasmalemma during the whole invasion process, as is the case with most protozoan parasites. Moreover, when a parasite uses phagocytosis to gain access into a cell, another important issue is its behavior facing the fate of a phagosome, i.e. fusion with a lysosome and exposure to a cocktail of lytic enzymes which are supposed to digest the phagosomal contents. Parasites seem to have also evolved various ways of escaping this fatal outcome, as will be described below. Different invasion processes which occur among intracellular eukaryotic pathogens are depicted in Fig. 1.

Because of their medical interest, host cell invasion by Apicomplexan zoites (e.g. Plasmodium, Toxoplasma, Eimeria, Sarcocystis, or Piroplasms) has been studied to a great extent (Apicomplexa/Host Cell Invasion).

In contrast, little morphological data are available on the invasion of host cells by kinetoplastids. More studies deal with the ways these organisms escape the phagosome lysosome fusion (Trypanosoma/Host Cell Invasion, Leishmania/Host Cell Invasion). Although rather poorly known, the mechanism of cell invasion by Microsporidia has very peculiar characteristics. Microsporidia self inject into their host cell by devaginating a membranous organelle (polar tube) which forces its way through the host cell plasmalemma and through which the parasite cytoplasm moves into the recipient cell (Fig. 1). Invasion is thus intrusive: this is the only case known among intracellular parasitic protozoa parasite development may occur either in the cytoplasm of the cell or within a parasitophorous vacuole; but whether this vacuoles forms at invasion or later is not known.



  
Fig. 1 Invasion processes observed among different intracellular pathogens. 1 Invasion by phagocytosis, parasite development in phagolysosomes (e.g. Leishmania spp.). 2 Invasion by “phagocytosis”, escape of the parasite into the host cell cytoplasm (e.g. Trypanosoma cruzi). 3, 4 Active invasion of Apicomplexa, characterized by a moving junction and the development of the parasitophorous vacuole. An originality of piroplasms (e.g. Babesia) is the disintegration of the parasitophorous vacuole membrane soon after invasion, the parasite then lying directly within the erythrocytic stroma (3). Other Apicomplexa complete their schizogony within a parasitophorous vacuole after inhibition of fusion with lysosomes (4). 5 Invasion through the host cell plasmalemma (Microsporidia).