Platelets in the pathogenesis of flavivirus disease.

Research on the role of platelets in modulating innate and adaptive host immune responses has gaining importance in the last two decades. Since the virus can directly interact with platelet receptors and modulate the host immune response, understanding the role of platelets in viral pathogenesis would pave way for novel therapeutic means. The present review aims at presenting the important molecular aspects of platelet-flavivirus interactions and how it leads to platelet activation, thrombocytopenia, and vascular endothelial leakage. Besides, the role of some of the platelet-derived factors as biomarkers for the early prediction of disease outcome taking dengue infection as an example is reviewed.

Altered Platelet Fatty Acids in Dengue Cases by Gas Chromatography-Mass Spectrometry Analysis.

BACKGROUND: The role of dengue virus in altering the functional properties of platelets remains poorly understood. Few studies have observed that changes in fatty acids are found to have an effect on platelet activation and aggregation. Also, platelet fatty acids have not been extensively studied in dengue so far. So, we aimed to study the fatty acids of platelet membranes in patients with dengue. METHODS: Gas chromatography-mass spectrometry (GC-MS) method was used to analyze fatty acids in the lipid extracts of platelets isolated from the study participants. RESULTS: GC-MS analysis of platelet lipids identified and quantified nearly 23 unique lipid molecules on platelet membrane. We observed significant alterations with some of the fatty acids in patients with dengue compared to controls. Within dengue cases, increase in unsaturated fatty acids in severe dengue was observed compared to non-severe dengue. From baseline to defervescence, no difference in fatty acids was observed in dengue platelets. This indicates that in dengue, platelet physiology remains altered even after the febrile phase. CONCLUSION: To the best of our knowledge, this is the first study characterizing the differential expression of platelet fatty acids in dengue infection. However, further studies are warranted to expound the underlying cause for thrombocytopenia and platelet dysfunction in dengue.

Lipid peroxidation, DNA damage, and apoptosis in dengue fever.

Interplay between the apoptosis, DNA damage, and oxidative stress as a host response to dengue viral infections remains unclear. Peripheral blood mononuclear cells (PBMCs) were isolated from 60 dengue infected patients, 20 patients with febrile illness other than dengue (OFI) and 10 non-febrile illness (NFI) patients. DNA damage in the PBMCs was assessed using single cell gel electrophoresis and stages of apoptosis underwent by the PBMCs were studied by Annexin-PI staining using flow cytometry. Plasma levels of malondialdehyde levels were estimated using thiobarbituric acid assay. Dengue infected individuals had showed increased DNA damage than NFI and OFI controls at the time of admission. Annexin-PI staining revealed increased frequency of apoptotic cells in dengue infected PBMCs than controls during the admission time. Similar pattern was observed in samples collected around defervescence. Within the dengue cases, percentage of live cells was higher in non-severe dengue than severe dengue at both the time points. Follow-up samples in dengue showed less number of live cells and higher percentage of apoptotic cells with respect to their baseline and this was reversed in case of OFI. Plasma malondialdehyde levels were found to be relatively higher in dengue cases than controls at admission and around defervescence. Significant positive correlation between DNA damage, apoptosis, and plasma malondialdehyde levels might pave a way for understanding the complex interactions between virus and hosts response thereby aids in identifying plausible immunopathological links contributing to disease pathogenesis. © 2018 IUBMB Life, 70(11):1133-1143, 2018.