Mycobacterium tuberculosis (Mtb), the hardy bacterial species that causes tuberculosis (TB), has an unexpected vulnerability that future drugs may be able to exploit, according to a study from researchers at Weill Cornell Medicine.
The researchers, whose findings appeared Nov. 15 in Nature Communications, investigated the role of an Mtb enzyme that had never been studied in depth before, and discovered that it is crucial for Mtb’s breakdown of available fatty acids to supply energy and molecular building blocks for growth and survival. Deleting just that one enzyme, which they called EtfDMtb, rendered Mtb unable to sustain an infection in mice.
“This enzyme is an attractive drug target for TB — silencing it not only starves the bacterium but also has an additional toxic effect on it,” said senior author Dr. Sabine Ehrt, a professor of microbiology and immunology at Weill Cornell…
