Abstract
Host cell invasion by apicomplexan parasites: the junction conundrum.
Highlights
Apicomplexans form a large phylum of parasitic protists, some of which cause severe diseases in humans
Zoites slide through the junction into an invagination of the host cell surface that becomes the parasitophorous vacuole (PV) after pinching off from the host cell plasma membrane, in a process that takes less than a minute
apical membrane antigen 1 (AMA1) vaccines have demonstrated protective efficacy in rodent and simian models against blood-stage challenge with the homologous strain [51], human vaccine trials using AMA1 have shown poor efficacy so far [52]. Both AMA1 and rhoptry neck proteins (RON) proteins are conserved in the apicomplexan phylum and the AMA1-RON complex has been detected in extracts from Toxoplasma tachyzoites and sporozoites [53], Plasmodium merozoites of various species [54], and Neospora [55]
Summary
Apicomplexans form a large phylum of parasitic protists, some of which cause severe diseases in humans. AMA1 vaccines have demonstrated protective efficacy in rodent and simian models against blood-stage challenge with the homologous strain [51], human vaccine trials using AMA1 have shown poor efficacy so far [52] Both AMA1 and RON proteins are conserved in the apicomplexan phylum and the AMA1-RON complex has been detected in extracts from Toxoplasma tachyzoites and sporozoites [53], Plasmodium merozoites of various species [54], and Neospora [55]. (iii) Antibodies or peptides that inhibit the AMA1–RON2 interaction reduce host cell invasion by Toxoplasma tachyzoites and Plasmodium merozoites [62,63,64,65] These results clearly pointed to the view that crossmembrane AMA1-RON2 complexes shaped the junction for zoite internalization [66,67] (Figure 1B).
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