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Arboviral Encephalitis

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...

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Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Tick-borne encephalitis--lipid peroxidation and its consequences.

Wojciech Łuczaj¹, Anna Moniuszko², Iwona Jarocka-Karpowicz¹

¹a Department of Analytical Chemistry , Medical University of Bialystok , Bialystok.

Scandinavian Journal of Clinical and Laboratory Investigation

|September 29, 2015

Summary

Lipid peroxidation is a key process in tick-borne encephalitis (TBE), indicated by elevated markers like 4-HNE and F2-isoprostanes. These lipid peroxidation products may aid in TBE diagnosis.

Keywords:

4-hydroxynonenal CSF MDA isoprostanes phospholipase A2 plasma urine

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Published on: March 26, 2019

Area of Science:

Biochemistry
Neuroscience
Pathophysiology

Background:

Tick-borne encephalitis (TBE) is a serious neurological disease.
Lipid peroxidation, a process involving damage to lipids, is implicated in TBE pathogenesis.
Prostaglandin derivatives and reactive aldehydes are key indicators of lipid peroxidation.

Purpose of the Study:

To assess lipid peroxidation processes in patients with TBE.
To identify major indicators of lipid peroxidation in cerebrospinal fluid (CSF), plasma, and urine of TBE patients.

Main Methods:

Analyzed 60 TBE patients and 56 healthy controls.
Measured lipid peroxidation markers including 4-hydroxynonenal (4-HNE), F2-isoprostanes, and neuroprostanes (NPs) using GC-MS and LC-MS.
Assessed activities of enzymes like phospholipase A2 (PLA2) and glutathione peroxidase (GSH-Px), and levels of fatty acids (arachidonic acid, linoleic acid, docosahexaenoic acid).

Main Results:

Observed significant decreases in arachidonic acid, linoleic acid, docosahexaenoic acid levels, and glutathione peroxidase activity in TBE patients.
Found markedly elevated plasma levels of F2-isoprostanes (7-fold) and CSF levels of neuroprostanes (3-fold) in TBE patients.
Detected increased levels of malondialdehyde (MDA), 4-HNE, and 4-hydroxyhexenal (4-HHE) in CSF, plasma, and urine of TBE patients, alongside altered PLA2 and platelet-activating factor acetylhydrolase (PAF-AH) activities.

Conclusions:

Lipid peroxidation plays a significant role in the pathophysiology of TBE.
Lipid peroxidation products show potential as diagnostic biomarkers for TBE.