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Historical outline
Published in David A Warrell, Herbert M Gilles, Essential Malariology, 2017
In 1901, Grassi had formulated the idea that there is a third, cryptic tissue phase following the inoculation of sporozoites by the bite of Anopheles. Raffaele in Italy was the first to demonstrate in 1934 the existence of this phase in bird malaria. Then, in 1948, the exo-erythrocytic stages, first of monkey malaria (Plasmodium cynomolgi) and then of human malaria (P. vivax), were discovered in the UK by Shortt and Garnham. This discovery explained what happens to the parasite during the incubation period and how the relapses of malaria infection occur.
Tafenoquine
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Tafenoquine (SB252263, previously known as WR 238605) is an investigational 8-aminoquinoline that is being co-developed as an antimalarial medication by Medicines for Malaria Venture and GlaxoSmithKline with the historical support of the US Army. Its structure is 2,6-dimethoxy-4-methyl-5-([3-trifluoromethyl]-phenoxy)-8-([4-amino-1-methylbutyl]amino) quinoline, as shown in Figure 181.1, with a formula of C24H28F3N3O3 · C4H6O4 and a molecular weight of 581.58 (succinate salt). It is better tolerated and can be given in higher dosages than its analog, primaquine. In clinical trials, tafenoquine has typically been formulated in tablet form containing 150, 200, or 400 mg of free base (188, 250, or 500 mg of succinate salt). Tafenoquine kills all stages of the malaria parasite and has demonstrated activity against Plasmodium falciparum and Plasmodium vivax in humans, as well as Plasmodium cynomolgi, Plasmodium berghei, and Plasmodium fragile in animals. Tafenoquine’s possible clinical indications could include the chemoprophylaxis of malaria, treatment of relapsing malaria, and blocking of malaria transmission. Its most common adverse events are gastrointestinal intolerance and transient elevation of liver enzymes, especially at the highest tolerated doses. Like primaquine, tafenoquine can cause severe hemolysis in persons deficient in glucose-6-phosphate dehydrogenase (G6PD) and causes a reversible elevation of methemoglobinemia. Its mechanism of action is unknown.
Contribution of Plasmodium immunomics: potential impact for serological testing and surveillance of malaria
Published in Expert Review of Proteomics, 2019
Kokouvi Kassegne, Eniola Michael Abe, Yan-Bing Cui, Shen-Bo Chen, Bin Xu, Wang-Ping Deng, Hai-Mo Shen, Yue Wang, Jun-Hu Chen, Xiao-Nong Zhou
Serological testing remains the gold standard for diagnosis in case biologic samples present some limitations or are unavailable. Plasmodium proteomics and immunomics have greatly helped improve profiling of antibody responses to identify promising sensitive and specific antigens for serological test purposes, especially in terms of cross-seroreactivity. With respect to Tables 1 and 2, orthologous genes in Pf and Pv have been identified to not sharing cross-reactive antigens reciprocally. For example, antigens encoded by PF3D7_0532100, PF3D7_0207000, and PF3D7_0930300, share orthologs in Pv, but have been shown to be recognized only in Pf infections; similarly, some Pv antigens (encoded by PVX_115450_1o2, PVX_090230_1o2, and PVX_087670_1o1) that have orthologs in Pf have been shown to be recognized in Pv mono-infections [45]. Also, leading non-orthologous species-specific antigens between these two species have been characterized (e.g. as PF3D7_0206800, PF3D7_1036400_e2s2, PVX_092995_2o2, PVX_097720, and PVX_003775_2o2). However, it is expected that further studies in more conventional assay formats validate their applicability. Thus, cross-seroreactivity with antigens that share common epitopes and which usually leads to false-positives and misdiagnosis could be significantly minimized or avoidable, especially in regions where more than one species of Plasmodium is endemic. In this context, it is worth noting that Pv-specific reactivity is extremely difficult to distinguish from Pf cross-reactivity in human populations, because individuals in most areas with Pv likely also have prior or co-exposure to Pf or other species. Thus, the inability to manipulate host immune responses and the importance of mono-infections, especially of Pv mono-infections, might mandate additional approaches, where animal models such as nonhuman primate (NHP) or rodent malaria models may be most appropriate [62,63]. NHP malarias are promising alternative models for humans, since many of the key human malaria syndromes and research problems have excellent primate models. Plasmodium cynomolgi is closely related and mimics the unique biology and pathogenesis of Pv [64], and the release of the genome sequence of this valuable primate malaria parasite promises for gene expression studies [65,66]. This species offers opportunities to study the dormant relapsing parasite forms (hypnozoites) and the unique infected RBC features of Pv [67,68], and help identify and understand the immune response behind host-parasite interactions. More so, the use of humanized rodent parasites carrying introduced genes from human vivax parasite to examining Pv proteins that do not have orthologs in Pf, may improve NHP models for dissecting human immune responses. This is of great importance, since it is possible that human hepatocytes and erythrocytes in rodents will allow the growth of human malaria parasites.