Rebekah L. Mokry

This study identifies glutamine as a carbon source for lipogenesis during HCMV infection through reductive carboxylation, contributing to lipidome remodeling.

This study shows HCMV increases phosphatidylcholine (PC) levels through de novo synthesis during early replication, independent of late gene expression.

This study shows HCMV infection reduces erucic acid levels, an antiviral fatty acid, by promoting metabolism that increases other fatty acids, thereby evading its antiviral effect.

This study shows that HCMV can replicate without glucose by using metabolites from upper glycolytic pathways like the pentose phosphate pathway.

This study compares HCMV replication efficiency in epithelial cells using viruses produced from fibroblasts or epithelial cells, finding higher titer and syncytia formation with epithelial-derived virus.

This study shows that HCMV can infect and replicate in terminally differentiated human cortical neurons, causing structural and functional changes including altered calcium signaling and neurotransmission.

The paper investigates how the source of HCMV affects neuronal pathogenesis in cerebral organoids and shows that neutralizing antibodies and neurotropic factors can mitigate gene expression dysregulation.