A study in the early, online edition of the Proceedings of the National Academy of Sciences suggests relationships forged through co-evolution between Helicobacter pylori bugs and their human hosts can significantly influence gastric disease risk. Researchers from the US and Colombia assessed genotyping patterns in pathogen and host blood samples taken from almost 250 individuals in two parts of Colombia with disparate gastric cancer rates but comparable H. pylori infection levels. Admixture and genomic variation turned up in pathogens and humans from both locales. But in individuals from the mountainous area, where gastric cancer rates are relatively high, investigators saw a greater proportion of European ancestry in H. pylori isolates, coupled with higher-than-average Amerindian ancestry in the human population. On the other hand, both H. pylori isolates and their human hosts tended to harbor a greater proportion of African ancestry in a coastal region of Colombia with lower gastric cancer rates.
The Broad Institute's Eric Lander and colleagues present a conceptual and analytical framework for tallying up heritability that stems from common variants and rare variants in another PNAS paper slated to appear online this week. The group compared and contrasted common variant association studies — performed under the umbrella term "genome-wide association studies" — with the sequencing studies used to search for rare variants contributing to a given disease or trait in an effort to provide a framework for designing such studies. For instance, results of their analysis indicated that the latter "rare variant association studies" would likely benefit from the same sorts of large sample sizes used to track down common risk variants.
An international team led by investigators at the US National Institutes of Health and the Houston Methodist Research Institute in Houston used genome-wide transcriptional profiling to gauge mouse immune responsesto Plasmodium yoelii infections involving two different strains of the malaria-causing parasite. The researchers' array-based gene expression analyses on spleen samples of P. yoelii-infected mice indicated that the malaria parasite prompts activity by different mouse innate immune response pathways depending on the strain involved. Results from follow-up knockdown and gene knockout experiments in the lab supported that notion, suggesting that the genetic background of a malaria parasite can influence both pathogenesis and the immune response elicited by an infected host.