Abstract
BackgroundThe development and propagation of malaria parasites in their vertebrate host is a complex process in which various host and parasite factors are involved. Sometimes the evolution of parasitaemia seems to be quelled by parasite load. In order to understand the typical dynamics of evolution of parasitaemia, various mathematical models have been developed. The basic premise ingrained in most models is that the availability of uninfected red blood cells (RBC) in which the parasite develops is a limiting factor in the propagation of the parasite population.Presentation of the hypothesisWe would like to propose that except in extreme cases of severe malaria, there is no limitation in the supply of uninfected RBC for the increase of parasite population.Testing the hypothesisIn this analysis we examine the biological attributes of the parasite-infected RBC such as cytoadherence and rosette formation, and the rheological properties of infected RBC, and evaluate their effects on blood flow and clogging of capillaries. We argue that there should be no restriction in the availability of uninfected RBC in patients.Implication of the hypothesisThere is no justification for the insertion of RBC supply as a factor in mathematical models that describe the evolution of parasitaemia in the infected host. Indeed, more recent models, that have not inserted this factor, successfully describe the evolution of parasitaemia in the infected host.
Highlights
Parasites often have a mechanism which regulates parasite load according to parasite density
Testing the hypothesis: In this analysis we examine the biological attributes of the parasiteinfected red blood cells (RBC) such as cytoadherence and rosette formation, and the rheological properties of infected RBC, and evaluate their effects on blood flow and clogging of capillaries
We argue that there should be no restriction in the availability of uninfected RBC in patients
Summary
Parasites often have a mechanism which regulates parasite load according to parasite density. Even in synchronous infection, rupture of segmenters and reinvasion takes well over one hour, suggesting that not all segmenters rupture at the same time These considerations indicate that complete clogging of the post capillary venules by cytoadhering PRBC is disadvantageous for the optimal propagation of the parasites. The availability of uninfected RBC to merozoites is not restrained As we have just argued, if total clogging of venules never occurs, does the availability of uninfected RBC limit the evolution of parasitaemia in non-immune patients as suggested by mathematical models of within-host parasite dynamics (see Introduction)? The anatomy of post capillary venules, the regulation of blood flow and cytoadherence of PRBC to the endothelium of the venules in conjunction with the parasite cycle, implies that reinvasion occurs in an open system In this system merozoites emerge from sequestered segmenters and are exposed to a continuous flow of uninfected RBC within the venule. Models of within host dynamics describing the dynamics of parasite evolution and auto-regulation that do not assume limitation of RBC availability were shown to successfully describe the clinical picture [65,66]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
