Abstract
Tick-borne encephalitis virus (TBEV) is the most prevalent arbovirus, with a tentative estimate of 10,000 to 10,500 infections occurring in Europe and Asia every year. Endemic in Northeast China, tick-borne encephalitis (TBE) is emerging as a major threat to public health, local economies and tourism. The complicated array of host physiological changes has hampered elucidation of the molecular mechanisms underlying the pathogenesis of this disease. System-level characterization of the serum metabolome and lipidome of adult TBEV patients and a healthy control group was performed using liquid chromatography tandem mass spectrometry. By tracking metabolic and lipid changes during disease progression, crucial physiological changes that coincided with disease stages could be identified. Twenty-eight metabolites were significantly altered in the sera of TBE patients in our metabolomic analysis, and 14 lipids were significantly altered in our lipidomics study. Among these metabolites, alpha-linolenic acid, azelaic acid, D-glutamine, glucose-1-phosphate, L-glutamic acid, and mannose-6-phosphate were altered compared to the control group, and PC(38:7), PC(28:3;1), TAG(52:6), etc. were altered based on lipidomics. Major perturbed metabolic pathways included amino acid metabolism, lipid and oxidative stress metabolism (lipoprotein biosynthesis, arachidonic acid biosynthesis, leukotriene biosynthesis and sphingolipid metabolism), phospholipid metabolism and triglyceride metabolism. These metabolites were significantly perturbed during disease progression, implying their latent utility as prognostic markers. TBEV infection causes distinct temporal changes in the serum metabolome and lipidome, and many metabolites are potentially involved in the acute inflammatory response and immune regulation. Our global analysis revealed anti- and pro-inflammatory processes in the host and changes to the entire metabolic profile. Relationships between metabolites and pathologies were established. This study provides important insight into the pathology of TBE, including its pathology, and lays the foundation for further research into putative markers of TBE disease.
Highlights
Tick-borne encephalitis (TBE) is a severe central nervous system infection caused by tickborne encephalitis virus (TBEV), a single-stranded, positive-sense RNA virus of the genus Flavivirus [1]
The serum metabolic markers obtained through metabolomics and lipidomics are displayed in S2 Fig. The filtered and normalized datasets obtained via LC-mass spectrometer (MS) analysis were used to create Principal component analysis (PCA) models to visualize the sample groupings (Fig 1)
The strongest response of patients to Tick-borne encephalitis virus (TBEV) infection occurred in the first 4 days of infection, and homeostasis recovery (RP) appeared around the fourth day of fever, accompanied by mild clinical symptoms, such as fever and headache; the acute phase (AP) accompanies with the course of encephalitis, which has been observed to come to a head during early febrile phase
Summary
Tick-borne encephalitis (TBE) is a severe central nervous system infection caused by tickborne encephalitis virus (TBEV), a single-stranded, positive-sense RNA virus of the genus Flavivirus [1]. TBEV is transferred by ticks parasitizing wild vertebrate hosts, primarily small mammals such as rodents and hedgehogs. Large animals, such as deer and horses are non-preferred hosts for TBEV. The second course of TBE occurs in 20–30% of infected patients and is marked by central nervous system symptoms of varying severity [1]. Tick-borne encephalitis virus (TBEV) is the most prevalent arbovirus, with a tentative estimate of 10,000 to 10,500 infections occurring in Europe and Asia every year. Endemic in Northeast China, tick-borne encephalitis (TBE) is emerging as a major threat to public health, local economies and tourism. The complicated array of host physiological changes has hampered elucidation of the molecular mechanisms underlying the pathogenesis of this disease
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