It is the disappearance of a glycolipid from the bacterial cell envelope during evolution that may have considerably increased the virulence of tuberculosis bacilli in humans. Scientists from the CNRS, the Institut Pasteur, and the Université Toulouse III – Paul Sabatier have shown that this disappearance modified the surface properties of Mycobacterium tuberculosis, favoring its aggregation in "cords" and increasing its pathogenicity. These findings, which enable a better understanding of the mechanisms linked to the evolution and pathogenic emergence of tuberculosis bacilli, constitute a major advance in our knowledge on this disease. The new findings were published online in Nature Microbiology on January 27, 2016. The article is titled "pks5-Recombination-Mediated Surface Remodelling in Mycobacterium tuberculosis Emergence.” Tuberculosis is a chronic bacterial disease caused by the infective agent Mycobacterium tuberculosis. In 2014, 9.6 million cases of tuberculosis and 1.5 million deaths were recorded throughout the world, meaning that this disease ranks second, after HIV/AIDS, among causes of death from a single infective agent (WHO, 2015). To fight tuberculosis, it is necessary to better understand the factors and mechanisms that favor its emergence and spread. The evolutionary stages and their associated genetic adaptations that enabled the tuberculosis bacillus to colonize humans are still little understood, unlike those of other infectious diseases such as plague or typhus. To address this issue, the researchers focused on another bacillus, Mycobacterium canettii, which is known to cause rare cases of tuberculosis and to be genetically close to the ancestor of M. tuberculosis. The team observed that colonies of these M. canetti bacteria differed markedly from those of M. tuberculosis bacilli.
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