Senecavirus A- and Non-Infected Cells at Early Stage of Infection: Comparative Metabolomic Profiles

Liu, Fuxiao; Ni, Bo; Wei, Rong

doi:10.3389/fcimb.2021.736506

Cited by 13 publications

(21 citation statements)

References 55 publications

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“…Some viruses, such as H1N1 influenza virus and MDV, have been reported to induce host glycolysis [ 16 , 37 ]. A recently reported bioinformatics analysis of metabolism in SVA infection showed that the virus can reprogram cellular glucose metabolism [ 38 ], in agreement with the experimental results presented here. CH-GDFS-2018 is a wild type virus isolated by our group in 2018 with recombinant features [ 39 ].…”

Section: Discussionsupporting

confidence: 91%

Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

Lin

et al. 2023

PLoS Pathog

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Senecavirus A (SVA)-induced porcine idiopathic vesicular disease has caused huge economic losses worldwide. Glucose metabolism in the host cell is essential for SVA proliferation; however, the impact of the virus on glucose metabolism in host cells and the subsequent effects are still unknown. Here, glycolysis induced by SVA is shown to facilitate virus replication by promoting lactate production, which then attenuates the interaction between the mitochondrial antiviral-signaling protein (MAVS) and retinoic acid-inducible gene I (RIG-I). SVA induces glycolysis in PK-15 cells, as indicated by significantly increased expression of hexokinase 2 (HK2), 6-phosphofructokinase (PFKM), pyruvate kinase M (PKM), phosphoglycerate kinase 1 (PGK1), hypoxia-inducible factor-1 alpha (HIF-1α), and superoxide dismutase-2 (SOD2) in a dose-and replication-dependent manner, and enhanced lactate production, while reducing ATP generation. Overexpression of PKM, PGK1, HIF-1α, and PDK3 in PK-15 cells and high glucose concentrations promote SVA replication, while glycolytic inhibitors decrease it. Inhibition of RLR signaling allowed better replication of SVA by promoting lactate production to attenuate the interaction between MAVS and RIG-I, and regulatory effect of glycolysis on replication of SVA was mainly via RIG-I signaling. SVA infection in mice increased expression of PKM and PGK1 in tissues and serum yields of lactate. Mice treated with high glucose and administered sodium lactate showed elevated lactate levels and better SVA replication, as well as suppressed induction of RIG-I, interferon beta (IFNβ), IFNα, interferon-stimulated gene 15 (ISG15), and interleukin 6 (IL-6). The inhibitory effect on interferons was lower in mice administered sodium oxamate and low glucose compared to the high glucose, indicating that RLR signaling was inhibited by SVA infection through lactate in vitro and in vivo. These results provide a new perspective on the relationship between metabolism and innate immunity of the host in SVA infection, suggesting that glycolysis or lactate may be new targets against the virus.

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Section: Discussionsupporting

confidence: 91%

Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

Lin

et al. 2023

PLoS Pathog

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“…Viruses are the most abundant and widely distributed biological entities worldwide, with varied genetic material and the ability to infect different species [ 29 ]. Furthermore, their lives depend on their host’s metabolism, including virion uncoating, genome replication, and progeny packaging [ 9 ]. The main purpose of the host’s metabolism is to convert nutrients into energy to sustain all cellular processes and provide raw materials for the biosynthesis of proteins, lipids, and nucleic acids.…”

Section: Discussionmentioning

confidence: 99%

“…Amino acids are crucial for living organisms. Many metabolomic studies have identified metabolic changes in amino acids caused by viral infections [ 9 , 40 , 41 ]. For example, murine norovirus controls the antiviral response by activating metabolic stress responses, which activate amino acid responses and impair inflammatory signaling [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…In nature, all viruses cannot replicate independently to produce offspring, and their life cycle is completely dependent on the host metabolism. After invading the host cells, the virus can significantly alter the cell’s metabolism [ 9 ]. Thus, it is necessary to determine how a cell’s metabolism is altered after viral infection, which would provide insight into the requirements of viral replication and reveal potential targets for viral inhibition [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

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Metabolomics Profiles Reveal New Insights of Herpes Simplex Virus Type 1 Infection

Huang

Wang

Lei

et al. 2023

IJMS

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Herpes simplex virus type 1 (HSV-1) is a ubiquitous human pathogen that can cause significant morbidity, primarily facial cold sores and herpes simplex encephalitis. Previous studies have shown that a variety of viruses can reprogram the metabolic profiles of host cells to facilitate self-replication. In order to further elucidate the metabolic interactions between the host cell and HSV-1, we used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to analyze the metabolic profiles in human lung fibroblasts KMB17 infected with HSV-1. The results showed that 654 and 474 differential metabolites were identified in positive and negative ion modes, respectively, and 169 and 114 metabolic pathways that might be altered were screened. These altered metabolites are mainly involved in central carbon metabolism, choline metabolism, amino acid metabolism, purine and pyrimidine metabolism, cholesterol metabolism, bile secretion, and prolactin signaling pathway. Further, we confirmed that the addition of tryptophan metabolite kynurenine promotes HSV-1 replication, and the addition of 25-Hydroxycholesterol inhibits viral replication. Significantly, HSV-1 replication was obviously enhanced in the ChOKα (a choline metabolic rate-limiting enzyme) deficient mouse macrophages. These results indicated that HSV-1 induces the metabolic reprogramming of host cells to promote or resist viral replication. Taken together, these observations highlighted the significance of host cell metabolism in HSV-1 replication, which would help to clarify the pathogenesis of HSV-1 and identify new anti-HSV-1 therapeutic targets.

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“…Six biological replicate samples were harvested for the metabolomics analysis. The metabolites were extracted as previously described (Liu et al, 2021). In brief, the samples were lysed with pre-cooled extraction buffer (methanol:acetonitrile:water, 2:2:1, v/v/v).…”

Section: Extraction Of Metabolomics Samplesmentioning

confidence: 99%

Comparative untargeted and targeted metabonomics reveal discriminations in metabolite profiles between Mycoplasma capricolum subsp. capripneumoniae and Mycoplasma capricolum subsp. capricolum

Hao,

Zhang,

Chen

et al. 2023

Front. Microbiol.

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BackgroundMycoplasmas are among the smallest prokaryotic microbes that can grow and proliferate on non-living media. They have reduced genomes, which may be associated with a concomitant reduction in their metabolic capacity. Mycoplasma capricolum subsp. capripneumoniae (Mccp) and Mycoplasma capricolum subsp. capricolum (Mcc), both belong to the Mycoplasma mycoides cluster, are significant important pathogenic Mycoplasma species in veterinary research field. They share high degree of genome homology but Mcc grows markedly faster and has higher growth titer than Mccp.MethodsThis study investigated the metabolites of these two pathogenic bacteria from the middle and late stages of the logarithmic growth phase through liquid chromatography–mass spectrometry–based metabolomics and targeted energy metabolomics. The multivariate analysis was conducted to identify significant differences between the two important Mycoplasma species.ResultsA total of 173 metabolites were identified. Of them, 33 and 34 metabolites involved in purine and pyrimidine, pyruvate metabolism, and amino acid synthesis were found to significantly differ in the middle and late stages, respectively. The abundance of fructose 1,6-bisphosphate, ADP, and pyruvate was higher in Mcc than in Mccp during the whole logarithmic period. Lactate was upregulated in slow-growing Mccp. The pH buffering agent N-[2-hydroxyethyl]piperazine-N′-[2-ethanesulfonic acid] added to media effectively prevented pH reduction and increase bacterial viability and protein biomass. The multivariate analysis revealed that the two Mycoplasma species significantly differed in glucose metabolism, growth factor transport and metabolism, cholesterol utilization, and environmental regulation.ConclusionThe study data are beneficial for understanding the metabolomic characteristics of these two crucial Mycoplasma species and shedding more light on mycoplasma metabolism, and serve as a resource for the pathogenesis and development of related vaccines.

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Senecavirus A- and Non-Infected Cells at Early Stage of Infection: Comparative Metabolomic Profiles

Cited by 13 publications

References 55 publications

Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

Senecavirus A-induced glycolysis facilitates virus replication by promoting lactate production that attenuates the interaction between MAVS and RIG-I

Metabolomics Profiles Reveal New Insights of Herpes Simplex Virus Type 1 Infection

Comparative untargeted and targeted metabonomics reveal discriminations in metabolite profiles between Mycoplasma capricolum subsp. capripneumoniae and Mycoplasma capricolum subsp. capricolum

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