An international team led by investigators at the University of Montana used genome and transcriptome sequencing to untangle some of the genes involved in a three-way symbiotic relationship involving Tremblaya princeps bacteria that live inside mealybugs and another bacterial species that acts as an endosymbiont to some that bacteria. Results of the researchers' assessment suggest the mealybug genome houses 22 or more genes nabbed from bacteria through horizontal gene transfer. But that gene set did not include genes from T. princeps, which apparently jettisoned some sequences from its compact genome after acquiring its own endosymbiont.
In one of two Cell papers using systems biology-based analyses to tease apart features of influenza infections, researchers from the US and Germany looked at gene expression profiles in sub-populations of cells from the lungs of influenza-infected mice. The work uncovered inflammatory pathways prone to activation in fatal influenza cases. In particular, study authors note, the experiments "provided clear evidence that lethality in this mouse model of acute influenza-induced death primarily does not arise directly from the cytopathic effects of the virus on non-hematopoietic cells, but rather from damage due to inadequately constrained innate inflammation primarily involving neutrophils co-acting with monocytes."
For a related Cell study, a team based at the University of California at San Diego, St. Jude Children's Research Hospital, and the University of Washington did lipidomic profiling in mice in an effort to find bioactive lipids mediating influenza-related inflammatory responses. Together with gene expression data, liquid chromatography and mass spectrometry-based lipidomic data pointed to distinct lipid patterns depending on the stage of influenza infection and the pathogenicity of the virus involved.