In Science Translational Medicine this week, researchers from Africa, the UK, and Australia report particular gene expression patterns are associated with severe cases of malaria. They sequenced RNA in blood samples from 46 Gambian children infected with Plasmodium falciparum — a parasite that causes severe malaria — and integrated their data with clinical information and estimates of parasite load. They find that children with more severe infection exhibited different patterns of gene expression compared to less severe cases. The researchers further discover that human differential gene expression in severe malaria was driven by differences in parasite load, while parasite gene expression showed little association with parasite load, as well as an association between neutrophil granule protein genes and severe malaria. "These findings provide a framework for understanding the contributions of host and parasite to the pathogenesis of severe malaria and identifying new treatments," they conclude. GenomeWeb has more on this, here.
Also in Science Translational Medicine, Princeton University researchers and their collaborators describe the creation of a genetically engineered mouse model for hepatitis delta virus (HDV) infection that better mimics how the virus functions in humans, as compared to alternative models. HDV, which causes chronic hepatitis delta (CHD), uses hepatitis B virus surface antigens to infect hepatocytes. By engineering a mice to express human receptor for HDV and HBV, the researchers were able to infect the animals' liver cells with HDV in a way that accurately represents the virus' life cycle. They also used their model to evaluate two investigational CHD treatments. "Our model is amenable to genetic manipulations, robust, and high in throughput, and thus lends itself for studying chronic hepatitis in vivo and systematically testing novel therapies targeting HDV," they write.