Abstract
Management of severe malaria remains a critical global challenge. In this study, using a multiplexed quantitative proteomics pipeline we systematically investigated the plasma proteome alterations in non-severe and severe malaria patients. We identified a few parasite proteins in severe malaria patients, which could be promising from a diagnostic perspective. Further, from host proteome analysis we observed substantial modulations in many crucial physiological pathways, including lipid metabolism, cytokine signaling, complement, and coagulation cascades in severe malaria. We propose that severe manifestations of malaria are possibly underpinned by modulations of the host physiology and defense machinery, which is evidently reflected in the plasma proteome alterations. Importantly, we identified multiple blood markers that can effectively define different complications of severe falciparum malaria, including cerebral syndromes and severe anemia. The ability of our identified blood markers to distinguish different severe complications of malaria may aid in developing new clinical tests for monitoring malaria severity.
Highlights
Management of severe malaria remains a critical global challenge
The following cohorts were included in the present study—Healthy control (HC), Nonsevere falciparum malaria (NSFM), Severe falciparum malaria (SFM), Cerebral malaria (CB), Severe anemia (SA), Control for severe anemia (CSA), Control for cerebral malaria (CCB), Nonsevere dengue fever (NSD), Severe dengue (SD), Non-severe vivax malaria (NSVM), and Severe vivax malaria (SVM)
Lower blood levels of Hb were observed in malaria patients [both falciparum malaria (FM) and VM], but no significant alteration was observed in dengue fever (DF) as compared to HC
Summary
Management of severe malaria remains a critical global challenge. In this study, using a multiplexed quantitative proteomics pipeline we systematically investigated the plasma proteome alterations in non-severe and severe malaria patients. We identified multiple blood markers that can effectively define different complications of severe falciparum malaria, including cerebral syndromes and severe anemia. Many population-based studies have shown partial or complete deletion of pfhrpII and pfhrpIII genes, which may lead to falsenegative results in RDTs17–19 Overall, these issues amply highlight the need for identification of additional parasite proteins and host factors for better diagnosis of malaria. The precise mechanisms that cause a transition from non-severe to severe fatal clinical manifestations in malaria, which often happens very rapidly, remains largely obscure. We performed comprehensive proteomics analysis of plasma samples from falciparum malaria patients with different severity levels and clinical manifestations to understand the mechanisms of malaria severity and its complications. We identified several blood-based host proteins marker for malaria severity and complexity, which can aid in monitoring disease progression. We have identified parasite proteins such as Serine Repeat Antigen 4 and Fructose-Bisphosphate Aldolase in severe malaria patients’
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