Abstract
Viral infections induce substantial metabolic changes in infected cells to optimize viral production while cells develop countermeasures to restrict that infection. Human respiratory syncytial virus (HRSV) is an infectious pathogen that causes severe lower respiratory tract infections (LRTI) in infants, the elderly, and immunocompromised adults for which no effective treatment or vaccine is currently available. In this study, variations in metabolite levels at different time points post-HRSV infection of epithelial cells were studied by untargeted metabolomics using liquid chromatography/mass spectrometry analysis of methanol cell extracts. Numerous metabolites were significantly upregulated after 18 hours post-infection, including nucleotides, amino acids, amino and nucleotide sugars, and metabolites of the central carbon pathway. In contrast, most lipid classes were downregulated. Additionally, increased levels of oxidized glutathione and polyamines were associated with oxidative stress in infected cells. These results show how HRSV infection influences cell metabolism to produce the energy and building blocks necessary for virus reproduction, suggesting potential therapeutic interventions against this virus.
Highlights
The relevance of metabolomics studies is increasingly recognized in many research areas, including host-pathogen interactions
Previous results from our group showed that Human respiratory syncytial virus (HRSV) infection had a profound time-dependent impact on the gene expression of infected cells, including the upregulation of many genes involved in protein biosynthesis, amino acid metabolism, response to oxidative stress, vitamin biosynthesis, RNA metabolism, cellular lipid metabolism, etc
We have focused on the metabolic changes induced by HRSV from 0 to 24 hours post-infection of epithelial cells
Summary
The relevance of metabolomics studies is increasingly recognized in many research areas, including host-pathogen interactions. Viruses are intracellular parasites that rely on cellular metabolism to obtain all the necessary structural and energetic resources for its replication. It is not surprising that viruses and infected cells have co-evolved to develop measures and countermeasures to promote or restrict virus replication, respectively. This battle results in a profound impact of virus infection on the host cell’s metabolism [1,2,3]. This dependence of viruses on cell metabolism provides new intervention opportunities for limiting virus replication
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