Reprogramming lipid metabolism in virus-infected neuronal cells

Exposure to environmental risk factors has been considered a major contributor to neurodegenerative diseases. As biological factors, infectious pathogens pose health concerns in the development of numerous aging-associated neurological defects. Emerging evidence continuously demonstrates the association between viral infection and the deterioration of brain function, such as dementia, multiple sclerosis, and microcephaly in infants. As intracellular pathogens, viruses demand macromolecules and energy by hijacking the host cell and reprogramming cellular metabolism. This study focuses on alterations in lipid metabolism in virus-infected neuronal cells using the DNA virus HSV-1 and the RNA virus ZIKV. We found that both HSV-1 and ZIKV downregulate lipid metabolism, sphingolipid metabolism, glycerophospholipid, and plasmalogen pathways in iPSC-derived neuronal cells, which may contribute to the pathogenesis of neurological diseases. The metabolomic dataset and analysis results will provide a valuable reference in studying the role of viral infection in neurodegeneration in vitro and in vivo .