The fusion of autophagosome with lysosome, to mature both structures in the autolysosome, is regulated by the SNARE complex, involving Syntaxin 17 (STX17)-located on the outer membrane of autophagosomes-synaptosomal-associated protein 29 (SNAP29), and vesicle-associated membrane protein 8 (VAMP8) on the lysosome outer membrane. LC3-II drives the growth and closure to form the complete autophagosome. Phagophore elongation requires the activities of two ubiquitin-like conjugation systems, comprising: (i) The ATG5–ATG12–ATG16L complex, which is assembled by the ligase action of ATG7 and ATG10 and (ii) LC3-PE (LC3-II), generated after the lipidation of phosphatidylethanolamine (PE) to LC3, a process facilitated by the ATG5–ATG12–ATG16L complex. The biogenesis of autophagosomes, double-membrane vesicles, initiates from the phagophore elongation followed by the closure of the edge of the membranes around the cytoplasmic material to be degraded. Therefore, the use of these species in rodent models has contributed greatly to the advancement in immunological and pathological research of human malaria. vinckei, present pathological conditions similar to the species that infect humans. Species that infect rodents but not humans, such as P. malariae, allowing progression to severe malaria and leading to serious health problems, especially in immunocompromised patients.

However, some studies have drawn attention to the growing virulence of P. ovale, it is associated with non-severe malaria.

vivax has a wider geographical distribution and, like P. falciparum can cause the most severe complications, such as anemia, cerebral, and placental malaria.

In humans, five species of Plasmodium are clinically relevant: Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, Plasmodium ovale (with two sub-species: Plasmodium ovale curtisi and Plasmodium ovale walikeri), and Plasmodium knowlesi.

Open in terminal killed silently in vnc