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This Week in PLOS: Feb 11, 2013

In PLOS One, researchers from the University of Massachusetts at Amherst and the University of Pennsylvania report on an analytical technique known as "mixed modeling of meta-analysis p-values," or MixMAP. The statistical method is designed to unearth associations at the locus level from existing data from genome-wide association studies, they say, by taking into account both SNP-level associations and genome structure. In the new study, for instance, the team tracked down 12 new gene-level loci suspected of influencing low density cholesterol data using information from a Global Lipids Gene Consortium GWAS, along with additional gene candidates ascertained using data from a smaller association study. See more on this study from our sister publication GenomeWeb Daily News.

Hantavirus may have appeared in bats or insectivorous animals before moving to rodent hosts, according to a new PLOS Pathogens study. A group of researchers based in China, Australia, and the US screened for hantavirus in hundreds of Chinese bats from several species as well as several dozen shrews from two species. That search uncovered four new hantaviruses, researchers report, while phylogenetic analyses of new and previously known hantaviruses pointed to the existence of at least four different hantavirus phylogroups infecting mammals. From relationships between the viruses, study authors also determined that "hantaviruses might have first appeared in Chiroptera (bats) or Soricomorpha (moles and shrews), before emerging in rodent species." "Our study shows that bats are likely to be important natural reservoir hosts of hantaviruses," they add, "from which novel hantaviruses may emerge in the future."

The Max Planck Institute for Molecular Genetics' Markus Morkel and colleagues from Germany describe regions of the mouse genome that become differentially methylated during colon cancer development. These loci are conserved to some extent in human forms of colon cancer, the investigators say in PLOS Genetics. They used methylated DNA immunoprecipitation coupled with high-throughput sequencing — or MeDIP-Seq — to test intestinal samples from mouse models of colon cancer, focusing first on benign adenoma precursors to disease. The team tracked down more than 13,000 sites in the genome with differential methylation in adenomas compared to normal controls. Follow-up experiments indicated that many of the same sites are also differentially methylated in human colon cancer. "Our data allow a distinction between early conserved epigenetic alterations occurring in intestinal adenoma and late stochastic events promoting colon cancer progression," the study's authors write, "and may facilitate the selection of more specific clinical epigenetic biomarkers."