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.
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Human infectious diseases are contributed
equally by the host immune
system’s efficiency and any pathogens’ infectivity.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the
coronavirus strain causing the respiratory pandemic coronavirus disease
2019 (COVID-19). To understand the pathobiology of SARS-CoV-2, one
needs to unravel the intricacies of host immune response to the virus,
the viral pathogen’s mode of transmission, and alterations
in specific biological pathways in the host allowing viral survival.
This review critically analyzes recent research using high-throughput
“omics” technologies (including proteomics and metabolomics)
on various biospecimens that allow an increased understanding of the
pathobiology of SARS-CoV-2 in humans. The altered biomolecule profile
facilitates an understanding of altered biological pathways. Further,
we have performed a meta-analysis of significantly altered biomolecular
profiles in COVID-19 patients using bioinformatics tools. Our analysis
deciphered alterations in the immune response, fatty acid, and amino
acid metabolism and other pathways that cumulatively result in COVID-19
disease, including symptoms such as hyperglycemic and hypoxic sequelae.
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