In PLOS Pathogens, a research duo from the University of Washington and the Fred Hutchinson Cancer Research Center reports on new clues about the evolution of simian immunodeficiency virus, a primate lentivirus related to HIV. Alex Compton and Michael Emerman searched for signs of lentivirus-related adaptation in Old World monkeys, looking in particular at the host gene APOBEC3G, which codes for a restriction factor interacting with a lentivirus encoded protein called Vif. From the available viral Vif patterns, coupled with information on APOBEC3G variability in the Old World monkeys, the investigators determined that animals in the lineage have been battling with lentiviruses from some five million to six million years or more. "Our analysis of virus-driven evolution describes an ancient yet ongoing genetic conflict between simian primates and lentiviruses on a million-year time scale," Compton and Emerman write.
Washington State University's Michael Skinner and his colleagues explore the cross-generational, epigenetic consequences of exposing pregnant rats to known or suspected endocrine-disrupting compounds in plastics during a stage of pregnancy at which gonadal sex determination is occurring in the developing embryo. As they report in PLOS One, the researchers identified differences in the predisposition for adult-onset diseases and obesity in multiple generations of rats descended from the endocrine disruptor-exposed group. The study authors also uncovered nearly 200 epigenetic shifts — or apparent epimutations — in sperm samples from rats in the F3 generation of the plastics treated lineage, prompting them to suggest that "sperm [differential DNA methylation regions] provide potential epigenetic biomarkers for transgenerational disease and/or ancestral environmental exposures."
A PLOS Genetics study highlights sites in the genome with newly detected ties to risk of B-cell lymphomas. A Memorial Sloan-Kettering Cancer Center-led team performed a two-stage genome-wide association study involving thousands of unaffected control individuals, individuals with sporadic lymphoma, or individuals with familial forms of lymphoma. After genotyping the top 50 SNPs falling out of the discovery stage of the study in almost 1,250 more cases and nearly 2,600 controls — and doing meta-analyses on data from all of the individuals with or without lymphoma — researchers identified some variants that seem to produce elevated risk of specific lymphomas and other SNPs with more general ties to multiple B-cell lymphoma subtypes.