Phytoplankton growth is sustained by the supply of essential nutrients and balanced by mortality processes such as viral infection, both of which can give rise to stress. Remod- elling of cellular lipids in response to such stresses is common in unicellular organisms. Under phosphorus (P) stress, phytoplankton substitute glycerophospholipids with non- phosphorus analogues, reducing their demand for P. Reported herein, the model marine diatom Thalassiosira pseudonana degraded only a small proportion of its original glyc- erophospholipid. Most of the P remained incorporated in glycerophospholipids, but significant changes in the individual glycerolipid species were observed. Untargeted lipidomic screening highlighted diglycosylceramides, not previously ob- served in T. pseudonana, that increase with P stress and may be useful as biomarkers. The fatty acids comprising each individual diglyceride lipid were characterised filling a conspicuous gap in our knowledge. Preliminary results suggest partitioning of diacylglyc- erol lipids between subcellular compartments. Marine diatoms, rich in lipids such as triacylglycerols are potential feedstocks for bio- fuels, where nitrogen (N) starvation is common to increase lipid yield. Quantification of individual glycerolipid species under N stress revealed that polyunsaturated glycerophos- phatidylcholine species and the predominant chemotype of sulfoquinovosyldiacylglycerol displayed large increases. Total diacylglycerol increased 3 fold under N stress, comprised of increases in saturated/monounsaturated species. This appears to form part of the cell’s adaption to N limitation that ultimately leads to the accumulation of triacylglycerides. These findings provide insight on the diatom lipidic response to nutrient stress and their adaptations to life in low nutrient environments, with additional implications upon biofuel production. Marine viruses infect phytoplankton influencing host ecology and evolution. Emilia- nia huxleyi has a biphasic life cycle with a diploid and haploid phase. Diploid cells are susceptible to infection by specific coccolithoviruses, yet haploid cells are resistant. Anal- ysis of lipids from cultures of uninfected diploid, infected diploid and uninfected haploid E. huxleyi revealed that sialic-glycosphingolipid, previously linked with susceptibility to infection, was absent from the resistant haploid cultures. Additional untargeted analyses unveiled potential biomarkers furthering our understanding of E. huxleyi host/virus lipid dynamics and highlight potential novel biomarkers for infection, susceptibility and ploidy.