Dysregulated metabolites and lipids in serum of patients with acute hepatitis E: A longitudinal study.
acute hepatitis
hepatitis E
lipid
longitudinal study
mass spectrometry
metabolite
Journal
Journal of viral hepatitis
ISSN: 1365-2893
Titre abrégé: J Viral Hepat
Pays: England
ID NLM: 9435672
Informations de publication
Date de publication:
Dec 2023
Dec 2023
Historique:
revised:
17
07
2023
received:
23
11
2022
accepted:
21
08
2023
medline:
17
11
2023
pubmed:
12
9
2023
entrez:
12
9
2023
Statut:
ppublish
Résumé
Hepatitis E is a disease associated with acute inflammation of the liver. It is related to several dysregulated metabolic pathways and alterations in the concentration of several metabolites. However, longitudinal analysis of the alterations in metabolites and lipids is generally lacking. This study investigated the changes in levels of metabolites and lipids over time in sera from men with acute hepatitis E compared to healthy controls similar in age and gender. Untargeted measurement of levels of various metabolites and lipids was done using mass spectrometry on 65 sera sequentially sampled from 14 patients with acute hepatitis E and 25 serum samples from five controls. Temporal changes in intensities of metabolites and lipids were determined over different times at 3-day periods for the hepatitis E virus (HEV) group. In carbohydrate metabolism, glucose levels, fructose 1-6-bisphosphate and ribulose-5-phosphate were increased in the HEV-infected persons compared to the healthy controls. HEV infection is significantly associated with decreased levels of inosine, guanosine, adenosine and urate in purine metabolism and thymine, uracil and β-aminoisobutyrate in pyrimidine metabolism. Glutamate, alanine and valine levels were significantly lower in the HEV group than in healthy individuals. Homogentisate of tyrosine metabolism and cystathionine of serine metabolism were increased, whereas kynurenate of tryptophan metabolism decreased in the HEV group. Metabolites of the bile acid biosynthesis, urea cycle (arginine and citrulline) and ammonia recycling (urocanate) were significantly altered. Co-enzymes, pantothenate and pyridoxal, and co-factors, lipoamide and FAD, were elevated in the HEV group. The acylcarnitines, sphingomyelins, phosphatidylcholine (PC), phosphatidylethanolamine (PE), lysoPC and lysoPE tended to be lower in the HEV group. In conclusion, acute hepatitis E is associated with altered metabolite and lipid profiles, significantly increased catabolism of carbohydrates, purines/pyrimidines and amino acids, and decreased levels of several glycerophospholipids.
Substances chimiques
Lipids
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
959-969Subventions
Organisme : Indian Council of Medical Research
Informations de copyright
© 2023 John Wiley & Sons Ltd.
Références
Khuroo MS. Chronic liver disease after non-a, non-Bhepatitis. Lancet. 1980;2:860-861.
Khuroo MS. Study of an epidemic of non-a, non-B hepatitis. Possibility of another human hepatitis virus distinct from post-transfusion non-a, non-B type. Am J Med. 1980;68(6):818-824.
Balayan MS, Andjaparidze AG, Savinskaya SS, et al. Evidence for a virus in non-a, non-B hepatitis transmitted via the fecal-oral route. Intervirology. 1983;20:23-31.
Hartl J, Wehmeyer MH, Pischke S. Acute hepatitis E: two sides of the same coin. Viruses. 2016;8(11):299.
Gupta N, Sarangi AN, Dadhich S, et al. Acute hepatitis E in India appears to be caused exclusively by genotype 1 hepatitis E virus. Indian J Gastroenterol. 2018;37(1):44-49.
Aslan AT, Balaban HY. Hepatitis E virus: epidemiology, diagnosis, clinical manifestations, and treatment. World J Gastroenterol. 2020;26(37):5543-5560.
Goel A, Padmaprakash KV, Benjamin M, Katiyar H, Aggarwal R. Temporal profile of HEV RNA concentration in blood and stool from patients with acute uncomplicated hepatitis E in a region with genotype 1 predominance. J Viral Hepat. 2020;27(6):631-637.
Nagashima S, Takahashi M, Kobayashi T, et al. Characterization of the quasi-enveloped hepatitis E virus particles released by the cellular Exosomal pathway. J Virol. 2017;91(22):e00822-17.
Taneja S, Sen S, Gupta VK, Aggarwal R, Jameel S. Plasma and urine biomarkers in acute viral hepatitis E. Proteome Sci. 2009;7(1):1-14.
Munshi SU, Taneja S, Bhavesh NS, Shastri J, Aggarwal R, Jameel S. Metabonomic analysis of hepatitis E patients shows deregulated metabolic cycles and abnormalities in amino acid metabolism: hepatitis E metabolomics. J Viral Hepat. 2011;18(10):e591-e602.
Wu J, Xu Y, Cui Y, et al. Dynamic changes of serum metabolites associated with infection and severity of patients with acute hepatitis E infection. J Med Virol. 2022;94(6):2714-2726.
Zhai L, Dai X, Meng J. Hepatitis E virus genotyping based on full-length genome and partial genomic regions. Virus Res. 2006;120(1-2):57-69.
Matyash V, Liebisch G, Kurzchalia TV, Shevchenko A, Schwudke D. Lipid extraction by methyl-tert-butyl ether for high-throughput lipidomics. J Lipid Res. 2008;49(5):1137-1146.
Koelmel JP, Kroeger NM, Ulmer CZ, et al. LipidMatch: an automated workflow for rule-based lipid identification using untargeted high-resolution tandem mass spectrometry data. BMC Bioinformatics. 2017;18(1):1-11.
Xia J, Psychogios N, Young N, Wishart DS. MetaboAnalyst: a web server for metabolomic data analysis and interpretation. Nucleic Acids Res. 2009;37:W652-W660.
Liebisch G, Fahy E, Aoki J, et al. Update on LIPID MAPS classification, nomenclature, and shorthand notation for MS-derived lipid structures. J Lipid Res. 2020;61(12):15391-15555.
Heaton NS, Randall G. Dengue virus-induced autophagy regulates lipid metabolism. Cell Host Microbe. 2010;8(5):422-432.
Keshavarz M, Solaymani-Mohammadi F, Namdari H, Arjeini Y, Mousavi MJ, Rezaei F. Metabolic host response and therapeutic approaches to influenza infection. Cell Mol Biol Lett. 2020;25(1):1-19.
Kawano Y, Cohen DE. Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease. J Gastroenterol. 2013;48(4):434-441.
Van Thiel DH, George M, Attar BM, Ramadori G, Ion-Nedelcu N. Plasma triglyceride levels may modulate hepatitis C viral replication. Dig Dis Sci. 2014;59(4):881-885.
Audi A, Soudani N, Dbaibo G, Zaraket H. Depletion of host and viral sphingomyelin impairs influenza virus infection. Front Microbiol. 2020;11:612.
Torretta E, Garziano M, Poliseno M, et al. Severity of COVID-19 patients predicted by serum sphingolipids signature. Int J Mol Sci. 2021;22(19):10198.
Kanno K, Wu MK, Scapa EF, Roderick SL, Cohen DE. Structure and function of phosphatidylcholine transfer protein (PC-TP)/StarD2. Biochim Biophys Acta. 2007;1771(6):654-662.
Payne AH, Hales DB. Overview of steroidogenic enzymes in the pathway from cholesterol to active steroid hormones. Endocr Rev. 2004;25(6):947-970.
Pikuleva IA. Cholesterol-metabolizing cytochromes P450. Drug Metab Dispos. 2006;34(4):513-520.
Miller M, Ginsberg HN, Schaefer EJ. Relative atherogenicity and predictive value of non-high-density lipoprotein cholesterol for coronary heart disease. Am J Cardiol. 2008;101(7):1003-1008.
Eisenreich W, Rudel T, Heesemann J, Goebel W. How viral and intracellular bacterial pathogens reprogram the metabolism of host cells to allow their intracellular replication. Front Cell Infect Microbiol. 2019;9:42.
Thaker SK, Chapa T, Garcia G Jr, et al. Differential metabolic reprogramming by zika virus promotes cell death in human versus mosquito cells. Cell Metab. 2019;29(5):1206-1216.
Ritter JB, Wahl AS, Freund S, Genzel Y, Reichl U. Metabolic effects of influenza virus infection in cultured animal cells: intra- and extracellular metabolite profiling. BMC Syst Biol. 2010;4(1):61.
Fonseca W, Malinczak CA, Schuler CF, et al. Uric acid pathway activation during respiratory virus infection promotes Th2 immune response via innate cytokine production and ILC2 accumulation. Mucosal Immunol. 2020;13(4):691-701.
Kuipers MT, Aslami H, Vlaar APJ, et al. Pre-treatment with allopurinol or uricase attenuates barrier dysfunction but not inflammation during murine ventilator-induced lung injury. PLoS One. 2012;7(11):e50559.
Jennings MR, Munn D, Blazeck J. Immunosuppressive metabolites in tumoral immune evasion: redundancies, clinical efforts, and pathways forward. J Immunother Cancer. 2021;9(10):e003013.
Leonardi R, Jackowski S. Biosynthesis of pantothenic acid and coenzyme A. EcoSal Plus. 2007;2(2). doi:10.1128/ecosalplus.3.6.3.4
Klassen P, Fürst P, Schulz C, Mazariegos M, Solomons NW. Plasma free amino acid concentrations in healthy Guatemalan adults and in patients with classic dengue. Am J Clin Nutr. 2001;73(3):647-652.
Shen B, Yi X, Sun Y, et al. Proteomic and metabolomic characterization of COVID-19 patient sera. Cell. 2020;182(1):59-72.
Luo L, Han W, Du J, et al. Chenodeoxycholic acid from bile inhibits influenza a virus replication via blocking nuclear export of viral ribonucleoprotein complexes. Molecules. 2018;23(12):3315.
Reese VC, Oropeza CE, McLachlan A. Independent activation of hepatitis B virus biosynthesis by retinoids, peroxisome proliferators, and bile acids. J Virol. 2013;87(2):991-997.
Cui L, Pang J, Lee YH, et al. Serum metabolome changes in adult patients with severe dengue in the critical and recovery phases of dengue infection. PLoS Negl Trop Dis. 2018;12(1):e0006217.
Diamond DL, Syder AJ, Jacobs JM, et al. Temporal proteome and lipidome profiles reveal hepatitis C virus-associated reprogramming of hepatocellular metabolism and bioenergetics. PLoS Pathog. 2010;6(1):e1000719.
Maceyka M, Spiegel S. Sphingolipid metabolites in inflammatory disease. Nature. 2014;510(7503):58-67.
Hu J, Zhang Z, Shen WJ, Azhar S. Cellular cholesterol delivery, intracellular processing and utilization for biosynthesis of steroid hormones. Nutr Metab (Lond). 2010;7(1):1-25.
Myo-Khin MK, Soe-Thein ST, Thein-Thein-Myint TTM, Than-Nu-Swe TNS, Tin-Tin-Saw TTS, Muya-Than MT. Serum cortisol levels in children with dengue haemorrhagic fever. J Trop Pediatr. 1995;41(5):295-297.
Mattner J, Debord KL, Ismail N, et al. Exogenous and endogenous glycolipid antigens activate NKT cells during microbial infections. Nature. 2005;434(7032):525-529.