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It’s a bitter irony that, for those in the global health community contending with viral outbreaks, many of the barriers to mounting an effective response are man-made. Geopolitical and cultural divides that separate us as people can inhibit research efforts and humanitarian aid. Viruses, meanwhile, pay little heed to such arbitrary boundaries; they prey instead on what we all have in common — our shared, human biology.

Nearly a decade ago, the FDA approved the drug lenalidomide to treat patients with deletion-5q myelodysplastic syndrome (del(5q) MDS), a cancer of the myeloid cells in the bone marrow that form several types of blood cells. In this condition, some bone marrow cells are missing a portion of chromosome 5 – hence, the “del(5q)” – on one copy of their genome (the human genome has two copies of each chromosome, one from each parent), and this deletion causes malignant cells to grow unchecked.

The number of copies of the AMY1 gene has been reported to influence metabolic response to diet, although this locus has been difficult to study. In a recent study published in Nature Genetics, Steve McCarroll and Joel Hirschhorn of the ӳý and Harvard Medical School and their colleagues show that eight common sets of genetic variants, or haplotypes, almost entirely explain the number of amylase gene copies in an individual. Yet to their surprise, there was no discernible relationship between obesity and copy number. The findings offer insights that could guide future investigations of other structurally complex loci in the genome.

Antibiotic resistance is a pressing concern worldwide. In order to prevent this bacterial insensitivity, it is critical to fully understand the antibiotics we currently use. A study published last week in the by researchers from the ӳý, MIT, Harvard University, and Massachusetts General Hospital focused on the ways in which antibiotics upset bacterial metabolism, as well as the effects of bacterial metabolism on antibiotics. Some antibiotics directly kill bacteria while others simply hinder growth — and not only can these two drug types interact, but they also impact cellular respiration differently. These findings suggest that susceptibility to antibiotics may be linked to bacterial metabolism.

ӳý of MIT and Harvard is teaming up with Google Genomics to explore how to break down major technical barriers that increasingly hinder biomedical research by addressing the need for computing infrastructure to store and process enormous datasets, and by creating tools to analyze such data and unravel long-standing mysteries about human health.