vivax and P. ovale, can then enter a period of latency by forming a non-replicating hypnozoite instead of a schizont. Over the course of 2 days to several days (dependent on species), a multinucleated exo-erythrocytic schizont (or meront) containing thousands of daughter merozoites forms. Once sporozoites have reached the liver sinusoids, they cross the sinusoidal barrier and enter into hepatocytes 2, in which they establish a parasitophorous vacuole and differentiate in a first round of asexual replication 4. The motile sporozoite enters the bloodstream, which enables it to reach the liver and thereby escape host immunity or drainage through the lymphatic system 2, 3. When an infected mosquito takes a blood meal from a vertebrate, it also injects sporozoites into the skin. The features of the malaria parasite life cycle are largely conserved across Plasmodium lineages that infect mammals (Fig. We put these findings in an evolutionary context and discuss new avenues for identifying drug targets and strategies to block transmission. In this Review, we discuss the biology of blood-stage malaria parasites, with a particular focus on recent breakthroughs in our understanding of the sexual stage and its development in the haematopoietic niche. Moreover, a series of studies have shown parasite replication and sexual differentiation in the haematopoietic niche of the vertebrate, which adds an unexpected, new feature to the parasite life cycle. In the past decade, renewed focus on sexual stages and transmission has unravelled pathways triggering their formation and unique cellular features. In most Plasmodium species, the highest cell numbers are reached during asexual replication in circulating blood cells of the vertebrate host a small fraction of those asexual parasites differentiate into sexual stages. Sexual stages (gametocytes) are always formed in blood cells in the vertebrate host, whereas gametogenesis and meiosis require transmission to the insect host. Malaria parasites have a complex life cycle marked by successive rounds of asexual replication across various stages and tissues, both in the intermediate vertebrate host and in the definitive insect host. Many other species of Plasmodium have been reported to cause malaria in vertebrates, including non-human primates (for example, Plasmodium cynomolgi in macaques and Plasmodium reichenowi in chimpanzees), rodents (for example, Plasmodium berghei and Plasmodium yoelli), birds (for example, Plasmodium gallinaceum, Plasmodium relictum and Plasmodium elongatum) and reptiles (for example, Plasmodium mexicanum). At least four additional species can infect humans: Plasmodium malariae, Plasmodium knowlesi, Plasmodium ovale curtisi and Plasmodium ovale wallikeri. Whereas Plasmodium falciparum dominates in sub-Saharan Africa, Plasmodium vivax is responsible for most cases in many regions of Asia. The past decade has seen a drastic reduction in malaria cases and deaths worldwide, but this stunning progress has now been halted by widespread emergence of drug resistance in both parasite and vector species. According to the WHO, 219 million malaria cases and 435,000 deaths worldwide were reported in 2017, with >90% of both cases and deaths in sub-Saharan Africa 1. Malaria is one of the major life-threatening infectious diseases in humans and is particularly prevalent in tropical and subtropical low-income regions of the world. Understanding these processes provides an opportunity for novel therapies and interventions. This Review focuses on our current understanding of blood-stage parasite development and vascular and tissue sequestration, which is responsible for disease symptoms and complications, and when involving the bone marrow, provides a niche for asexual replication and gametocyte development. The bone marrow, in particular the haematopoietic niche (in rodents, also the spleen), is a major site of parasite growth and sexual development. A few of these blood-stage parasites make a developmental switch into the sexual stage (or gametocyte), which is essential for transmission. Following one asexual amplification cycle in the liver, parasites reach high burdens by rounds of asexual replication within red blood cells. This diversity is testament to their exceptional adaptability and poses a major challenge for developing effective strategies to reduce the disease burden and transmission. They grow and develop in a wide range of host environments, both within blood-feeding mosquitoes, their definitive hosts, and in vertebrates, which are intermediate hosts. parasites are the causative agents of malaria in humans and animals, and they are exceptionally diverse in their morphology and life cycles.
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