Cellular Metabolomics of Rhabdomyosarcoma Cell during Echovirus 30Infection

Abstract

The Human echovirus 30 causes acute aseptic meningitis. Viral replication requires energy and macromolecular precursors derived from the metabolic network of the host cell. The effect of viral infection within a host cell metabolic activity remains unclear. To study an insight of cell-virus interaction during echovirus 30 infection we used human rhabdomyosarcoma cell line. The new approach of metabolomics the 1H NMR was used to measure the level of various cellular metabolites at different times of infections and morphological examination of the cells. The 1H NMR metabolite spectrum signals were observed between uninfected and infected cells. Both uninfected and infected cells utilized the glucose through metabolic pathways and released the metabolic end products. After infection the concentration of Alanine, Lactate, Acetate, Glutamate, Tyrosine, Histidine, Phenylalanine, Creatine, Choline and Formate, were increased and all these augmented metabolites were decreased at the end of the infection. The cells showed wide-ranging lipid signals at the end of the infections, which correlates with the morphological changes as apoptosis of cells was observed. Progressive breakdown and utilization of all cellular components were observed as the infections were increased. This study is useful for monitoring the cellular metabolic changes during virus infection.