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Multi-platform omics analysis of Nipah virus infection reveals viral glycoprotein modulation of mitochondria: metabolomics

ABSTRACT: We analyzed changes in cellular components and processes during NiV infection through a time-course exposure using live virus and individual genes (or combinations) via transfection. Our multi-omics approach has displayed an enrichment in mitochondrial proteins. This enrichment phenotype was also observed when we combine viral glycoprotein genes in transfection experiments. These analyses provide an atlas of cellular changes during NiV infections, helpful in designing therapeutics against rapidly growing Henipavirus genes and related infections.

INSTRUMENT(S): Agilent 7890A GC with 5975C inert XL MSD

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Joshua N. Adkins Hector Aguilar-Carreno

PROVIDER: MSV000086735 | MassIVE | Wed Jan 20 11:37:00 GMT 2021

REPOSITORIES: MassIVE

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Project description:MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection. Control (mock-infected) samples: 12 (2 technical replicates, averaged), Infected samples: 6, for each time-point (0, 4, 8, 24, 48 and 72 hours post infection). The experiment was performed in six replicates.

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Multi-platform omics analysis of Nipah virus infection reveals viral glycoprotein modulation of mitochondria: metabolomics

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