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Distinct amino acid and lipid perturbations characterize acute versus chronic malaria
Regina Joice Cordy, … , Alberto Moreno, Mary R. Galinski
Regina Joice Cordy, … , Alberto Moreno, Mary R. Galinski
Published May 2, 2019
Citation Information: JCI Insight. 2019;4(9):e125156. https://doi.org/10.1172/jci.insight.125156.
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Research Article Infectious disease Microbiology

Distinct amino acid and lipid perturbations characterize acute versus chronic malaria

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Abstract

Chronic malaria is a major public health problem and significant challenge for disease eradication efforts. Despite its importance, the biological factors underpinning chronic malaria are not fully understood. Recent studies have shown that host metabolic state can influence malaria pathogenesis and transmission, but its role in chronicity is not known. Here, with the goal of identifying distinct modifications in the metabolite profiles of acute versus chronic malaria, metabolomics was performed on plasma from Plasmodium-infected humans and nonhuman primates with a range of parasitemias and clinical signs. In rhesus macaques infected with Plasmodium coatneyi, significant alterations in amines, carnitines, and lipids were detected during a high parasitemic acute phase and many of these reverted to baseline levels once a low parasitemic chronic phase was established. Plasmodium gene expression, studied in parallel in the macaques, revealed transcriptional changes in amine, fatty acid, lipid and energy metabolism genes, as well as variant antigen genes. Furthermore, a common set of amines, carnitines, and lipids distinguished acute from chronic malaria in plasma from human Plasmodium falciparum cases. In summary, distinct host-parasite metabolic environments have been uncovered that characterize acute versus chronic malaria, providing insights into the underlying host-parasite biology of malaria disease progression.

Authors

Regina Joice Cordy, Rapatbhorn Patrapuvich, Loukia N. Lili, Monica Cabrera-Mora, Jung-Ting Chien, Gregory K. Tharp, Manoj Khadka, Esmeralda V.S. Meyer, Stacey A. Lapp, Chester J. Joyner, AnaPatricia Garcia, Sophia Banton, ViLinh Tran, Viravarn Luvira, Siriwan Rungin, Teerawat Saeseu, Nattawan Rachaphaew, Suman B. Pakala, Jeremy D. DeBarry, MaHPIC Consortium, Jessica C. Kissinger, Eric A. Ortlund, Steven E. Bosinger, John W. Barnwell, Dean P. Jones, Karan Uppal, Shuzhao Li, Jetsumon Sattabongkot, Alberto Moreno, Mary R. Galinski

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Figure 1

Longitudinal rhesus macaque infections with P.

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Longitudinal rhesus macaque infections with P.

coatneyifrom acute to ch...
coatneyifrom acute to chronic disease. (A) Time course of parasitemia (black dots) and hemoglobin concentrations (red dots) in 4 rhesus macaques (animal codes: RTi13, RUn13, RZe13, and RWr13), with time points (TPs) denoted by orange vertical lines. Rx indicates subcurative treatment with artemether. (B) Rectal temperature across disease phases (mean ± SEM, N = 4) with normal range shown in yellow. *P < 0.05 by repeat-measures ANOVA with Bonferroni’s correction. (C) Median number of hematopoietic progenitors in the BM at each phase, per animal, for erythroid (red) and myeloid (orange) progenitors. PP, pre-patent; A, acute; PS, post-subcurative treatment; C, chronic.

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