Abstract
Plasmodium, Toxoplasma, Cryptosporidium, Babesia, and Theileria are the major apicomplexan parasites affecting humans or animals worldwide. These pathogens represent an excellent example of host manipulators who can overturn host signaling pathways for their survival. They infect different types of host cells and take charge of the host machinery to gain nutrients and prevent itself from host attack. The mechanisms by which these pathogens modulate the host signaling pathways are well studied for Plasmodium, Toxoplasma, Cryptosporidium, and Theileria, except for limited studies on Babesia. Theileria is a unique pathogen taking into account the way it modulates host cell transformation, resulting in its clonal expansion. These parasites majorly modulate similar host signaling pathways, however, the disease outcome and effect is different among them. In this review, we discuss the approaches of these apicomplexan to manipulate the host–parasite clearance pathways during infection, invasion, survival, and egress.
Highlights
The Apicomplexan parasites represent a major class of pathogens with a wide host range
We focus on the potential sabotage mechanisms adopted by the five well-studied pathogens of human and veterinary importance: Plasmodium falciparum, Babesia bovis, Theileria annulata, Toxoplasma gondii, and Cryptosporidium parvum
It is apparent that few of the host defense pathways targeted by these parasites to survive and proliferate in the host cell are common among the mentioned pathogens
Summary
The Apicomplexan parasites represent a major class of pathogens with a wide host range They have emerged as one of the most successful intracellular parasites, which efficiently modulate the host for their survival benefits. We focus on the potential sabotage mechanisms adopted by the five well-studied pathogens of human and veterinary importance: Plasmodium falciparum (malaria), Babesia bovis (babesiosis), Theileria annulata (theileriosis), Toxoplasma gondii (toxoplasmosis), and Cryptosporidium parvum (cryptosporidiosis). These parasites are morphologically similar; variations exist in the context of host range, mode of infection, invasion, and replication inside the host (Table 1). We epitomize the major blueprint of the pathways targeted by these parasites to sabotage the host defense mechanism for their survival and consequent disease progression
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