In a study published in the journal Proceedings of the National Academy of Sciences (PNAS), researchers from the Institute for Systems Biology and Seattle BioMed identified the protein phosphotyrosine post-translational modifications critical to the growth of Mycobacterium tuberculosis (Mtb), a pathogen that causes the highly infectious disease tuberculosis (TB).
It may not be marked on your calendar, but today, March 24 is World TB Day , created to remind people of the massive global health problem caused by tuberculosis. On this day in 1882, the brilliant microbiologist Dr. Robert Koch announced his stunning discovery that TB is caused by infection with a bacterium,Mycobacterium tuberculosis. At the time, TB killed one in seven people in Europe and the Americas. Now, 132 years later, TB still kills more people than any other infection save AIDS – and many AIDS patients worldwide actually die of TB. Why does TB continue to rage despite decades of scientific progress, and why am I nonetheless hopeful that great improvements in stopping TB are possible?
Despite decades of research on the bacterium that causes tuberculosis (TB), scientists have not had a comprehensive understanding of how the bacterium is wired to adapt to changing conditions in the host. Now, researchers at Stanford University, Seattle BioMed, Boston University and the Broad Institute, Max Planck Institute of Biology in Berlin, Germany, Caprion Proteomics Inc. in Montreal, Canada, Brigham and Woman’s Hospital (Harvard University), and Colorado State University have taken the first steps toward a complete representation of the regulatory network for Mycobacterium tuberculosis. This map of the network of genes that control the TB bacterium will yield unique insights into how the bacteria survive in the host, and how they can be tackled with new drug interventions. The landmark results are published this week in the journal Nature.