Apicomplexan parasites are obligate intracellular protozoans that can cause severe human and animal diseases, such as malaria, toxoplasmosis, cryptosporidiosis, neosporosis, coccidiosis, etc. These parasites have evolved complex lifecycles, which consist of asexual and sexual stages to maintain their transmission and persistence in a wide range of hosts via adaption to different host niches. Apicomplexan parasites undergo multiple rounds of lytic cycle within host cells to proliferate. Lytic cycle of these parasites comprises of four major events: gliding motility, invasion, replication and egress, which are temporally and spatially regulated by a series of signaling pathways, especially calcium signaling cascade. Apicomplexan parasites utilize a substrate-dependent gliding motility to move and to drive invasion and egress from the infected cells. Parasites actively invade host cells in a sophisticated manner dependent on subsequential release of secretory proteins from specialized apical organelles. During host cell entry, parasitophorous vacuole (PV) is formed as a protective niche wherein parasite replication ensues. Parasites egress from the infected host cells to maintain multiplication and disseminate in the hosts.
Apicomplexan PV is the host-parasite interaction frontier that can be modified by rhoptry proteins (ROPs) and dense granule proteins (GRAs) to compromise host cell defense systems and to scavenge nutrients from host cells. Parasites secrete many effectors including ROPs and GRAs to manipulate host cell signaling pathways. These effectors can be either targeted to PVM or injected into host cells, contributing to pathogen virulence and survival by overcoming host defense. In additional to the key role in physical barrier against host cell defense mechanism, PV membrane (PVM) functions as a molecular sieve to allow the passive transport of small nutrient molecules such as amino acids, purines, and lipids. This directly establishes a metabolic bridge between host and parasite. Some apicomplexan PVMs recruit host cell metabolic organelles including mitochondria and ER possibly to ensure nutrient acquisition and potentially to regulate host cell metabolism.
The overall goal of this Research Topic is to inspire and bring together new ideas, opinions and views that can not only advance our understanding of metabolic and immune adaptations of intracellular infection by apicomplexan parasites but expand our knowledge on the comprehensive interactions between host and apicomplexan parasites.
For this topic, we aim to collect novel studies on the interactions between host and apicomplexan parasites and welcome all types of articles including Original Research, Reviews, Mini-Reviews, Methods, Perspectives, Brief Research Reports that cover, but not limited to the following topics:
1. Regulation mechanism of lytic cycle
2. Subversion of host cell signaling pathways by parasites
3. Suppression and eradication of parasites by host cells
4. Acquisition of host nutrients by parasites
5. Remodeling of host metabolism by parasites
Apicomplexan parasites are obligate intracellular protozoans that can cause severe human and animal diseases, such as malaria, toxoplasmosis, cryptosporidiosis, neosporosis, coccidiosis, etc. These parasites have evolved complex lifecycles, which consist of asexual and sexual stages to maintain their transmission and persistence in a wide range of hosts via adaption to different host niches. Apicomplexan parasites undergo multiple rounds of lytic cycle within host cells to proliferate. Lytic cycle of these parasites comprises of four major events: gliding motility, invasion, replication and egress, which are temporally and spatially regulated by a series of signaling pathways, especially calcium signaling cascade. Apicomplexan parasites utilize a substrate-dependent gliding motility to move and to drive invasion and egress from the infected cells. Parasites actively invade host cells in a sophisticated manner dependent on subsequential release of secretory proteins from specialized apical organelles. During host cell entry, parasitophorous vacuole (PV) is formed as a protective niche wherein parasite replication ensues. Parasites egress from the infected host cells to maintain multiplication and disseminate in the hosts.
Apicomplexan PV is the host-parasite interaction frontier that can be modified by rhoptry proteins (ROPs) and dense granule proteins (GRAs) to compromise host cell defense systems and to scavenge nutrients from host cells. Parasites secrete many effectors including ROPs and GRAs to manipulate host cell signaling pathways. These effectors can be either targeted to PVM or injected into host cells, contributing to pathogen virulence and survival by overcoming host defense. In additional to the key role in physical barrier against host cell defense mechanism, PV membrane (PVM) functions as a molecular sieve to allow the passive transport of small nutrient molecules such as amino acids, purines, and lipids. This directly establishes a metabolic bridge between host and parasite. Some apicomplexan PVMs recruit host cell metabolic organelles including mitochondria and ER possibly to ensure nutrient acquisition and potentially to regulate host cell metabolism.
The overall goal of this Research Topic is to inspire and bring together new ideas, opinions and views that can not only advance our understanding of metabolic and immune adaptations of intracellular infection by apicomplexan parasites but expand our knowledge on the comprehensive interactions between host and apicomplexan parasites.
For this topic, we aim to collect novel studies on the interactions between host and apicomplexan parasites and welcome all types of articles including Original Research, Reviews, Mini-Reviews, Methods, Perspectives, Brief Research Reports that cover, but not limited to the following topics:
1. Regulation mechanism of lytic cycle
2. Subversion of host cell signaling pathways by parasites
3. Suppression and eradication of parasites by host cells
4. Acquisition of host nutrients by parasites
5. Remodeling of host metabolism by parasites
