Dataset Information

Gene expression changes in liver upon LCMV Cl13 infection.

ABSTRACT: 2-3 month old female C57Bl/6J mice were intravenously infected with 2x10^6 focus forming units of lymphocytic choriomeningitis virus strain Clone-13. Whole liver tissue was harvested in duplicated from uninfected control mice, uninfected 123d old mice, and from infected at 2, 8, 30, 60, and 123 days post infection. Three TMT 6-plex runs were carried out to monitor the changes in liver protein abundance during the entire course of infection. The first run included samples from day 2 and day 8 after infection along with the uninfected controls. Similarly, the second run included uninfected controls and samples from day 30 and day 60 after infection. The third run included samples day 123 after infection, the corresponding age matched control that was left uninfected for 123 days and the uninfected controls used in the other two runs. The uninfected controls were included in all the three runs as an internal control to monitor reproducibility between the runs.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Alexandra Popa

LAB HEAD: Dr. Andreas Bergthaler

PROVIDER: PXD011122 | Pride | 2019-12-02

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	M447-A01-O199-MM-P5186-1.raw	Raw
	M447-A02-O199-MM-P5186-1.raw	Raw
	M447-A03-O199-MM-P5186-1.raw	Raw
	M447-A04-O199-MM-P5186-1.raw	Raw
	M447-A05-O199-MM-P5186-1.raw	Raw

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Publications

Type I Interferon Signaling Disrupts the Hepatic Urea Cycle and Alters Systemic Metabolism to Suppress T Cell Function.

Lercher Alexander A Bhattacharya Anannya A Popa Alexandra M AM Caldera Michael M Schlapansky Moritz F MF Baazim Hatoon H Agerer Benedikt B Gürtl Bettina B Kosack Lindsay L Májek Peter P Brunner Julia S JS Vitko Dijana D Pinter Theresa T Genger Jakob-Wendelin JW Orlova Anna A Pikor Natalia N Reil Daniela D Ozsvár-Kozma Maria M Kalinke Ulrich U Ludewig Burkhard B Moriggl Richard R Bennett Keiryn L KL Menche Jörg J Cheng Paul N PN Schabbauer Gernot G Trauner Michael M Klavins Kristaps K Bergthaler Andreas A

Immunity 20191126 6

Infections induce complex host responses linked to antiviral defense, inflammation, and tissue damage and repair. We hypothesized that the liver, as a central metabolic hub, may orchestrate systemic metabolic changes during infection. We infected mice with chronic lymphocytic choriomeningitis virus (LCMV), performed RNA sequencing and proteomics of liver tissue, and integrated these data with serum metabolomics at different infection phases. Widespread reprogramming of liver metabolism occurred ...[more]

PMID: 31784108

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Project description:Rhesus macaques (Macaca mulatta) infected with a lethal dose of lymphocytic choriomeningitis virus-strain WE (LCMV-WE) provide a model for Lassa fever virus infection of man. Like Lassa fever in human beings, disease begins with flu-like symptoms but can progress to morbidity fairly rapidly. Previously, we profiled the blood transcriptome of LCMV-infected monkeys (M. Djavani et al. J. Virol. 2007: PMID 17522210) showing distinct pre-viremic and viremic stages that discriminated between virulent and benign infections. In the present study, changes in liver gene expression from macaques infected with virulent LCMV-WE were compared to gene expression in uninfected monkeys as well as to monkeys that were infected but not diseased. We observed gene expression changes that occurred before the viremic stage of the disease, and could potentially serve as biomarkers that discriminate between exposure to a hemorrhagic fever virus and exposure to a benign virus. Based on a functional pathway analysis of differentially expressed genes, virulent LCMV-WE had a much broader effect on liver cell function than non-virulent virus. During the first few days of infection, virulent virus impacted gene expression associated with the generation of energy, such as fatty acid metabolism and glucose metabolism, with the complement and coagulation cascades, and with steroid metabolism, MAPK signaling and cell adhesion. For example, the energy profile resembled that of an organism entering starvation: acetyl-CoA carboxylase, a key enzyme of fatty acid synthesis, was shut down and gene products involved in gluconeogenesis were up-regulated. In conclusion, this study identifies several potential gene markers of LCMV-WE-associated liver disease and contributes to the database of gene expression changes correlated with LCMV pathogenesis in primates. 6 groups: uninfected controls, LCMV-WE infected (pre-viremic; day 1 to day 3), LCMV-WE infected (viremic; day 4 to day 7), LCMV-WE infected (post-viremic; day 8 to day 12), LCMV-Armstrong (LCMV-ARM; non-virulent strain) infected, and LCMV-ARM/LCMV-WE infected but not diseased. Each sample is from the liver of a different rhesus macaque.