Abstract
BackgroundWe present two conundra in the biology of intraerythrocytic malaria parasite: how an apparent open parasitophorous duct provide direct access of only a select set of serum proteins to the parasitophorous vacuole, and how proteases mediate membrane lysis to allow merozoite egress.SolutionWe posit the existence of a parasitophorous vacuolar duct plug that is originally formed from a tight junction (or parts thereof) between merozoite apical surface and red blood cell plasma membrane, which by moving over the parasite surface towards the posterior end draws the parasite into the host cell interior, and by remaining at the passage orifice provides a location of transporter(s) for import of serum proteins into parasitophorous vacuole and an opening for merozoite egress upon its dissolution/dismantling through protease(s) action.ConclusionThis notion obviates the need of a distinct intact parasitophorous vacuolar membrane, which in the proposed model is an extension of the red blood cell membrane but still forms an intracellular compartment for parasite growth and development. The model is testable using existing high-resolution electron and X-ray tomography tools.
Highlights
We present two conundra in the biology of intraerythrocytic malaria parasite: how an apparent open parasitophorous duct provide direct access of only a select set of serum proteins to the parasitophorous vacuole, and how proteases mediate membrane lysis to allow merozoite egress.Solution: We posit the existence of a parasitophorous vacuolar duct plug that is originally formed from a tight junction between merozoite apical surface and red blood cell plasma membrane, which by moving over the parasite surface towards the posterior end draws the parasite into the host cell interior, and by remaining at the passage orifice provides a location of transporter(s) for import of serum proteins into parasitophorous vacuole and an opening for merozoite egress upon its dissolution/dismantling through protease(s) action
Two recent publications in this Journal have recently demonstrated direct access of intraerythrocytic Plasmodium falciparum to a selective group of serum proteins via a process independent of passage through infected red blood cell (RBC) cytosol, namely, that of prothrombin, vitamin K-dependent protein S, and vitronectin reported by Tougan et al [1], who identified the presence of such proteins by shotgun liquid chromatography-mass spectrometry/mass spectrometry, western blotting and confocal microscopy of fluorescent-tagged proteins, and that of plasminogen reported by Maluf et al [2] employing immunogold electron microscopy and western blotting
The most glaring weakness of the existence of a parasitophorous duct is the requirement of an opening at the infected RBC surface of a defined diameter to allow entry of macromolecules into the parasite parasitophorous vacuole (PV), but without any explanation for the necessary regulation of a consequential intermingling of PV non-macromolecular content with the external milieu, let alone the osmotic pressure arising from an opening at a cell surface
Summary
This notion obviates the need of a distinct intact parasitophorous vacuolar membrane, which in the proposed model is an extension of the red blood cell membrane but still forms an intracellular compartment for parasite growth and development.
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