Elucidating the role of mycobacterial secreted phosphatases in host lipid dynamics and pathogen survival

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Tuberculosis (TB) is one of the oldest and most persistent bacterial infectious diseases that affects humans. Despite significant advances to control the spread of TB with the introduction of vaccines and antibiotics, one third of the human population is still infected, and 1.6 million die every year. The rise in drug resistance and the limited arsenal of effective antibiotics is threatening to further expand the disease burden. New therapeutic approaches are urgently needed to fight the disease. Mycobacterium tuberculosis (Mtb), the causing agent of TB, is able to challenge our immune system and to survive in the lungs by evading our natural defences. Generally, our white blood cells will engulf and digest microbes to stop infections, in a process known as phagocytosis. However, TB produces a number of substances, "survival factors", that stop this process allowing the bacteria to grow and multiply inside the white blood cells and then spread to nearby cells. The precise mechanisms that allow the bacteria to survive are still poorly understood. We now want to understand how these survival factors work and what happens when we block their action. A better understanding of these processes will help us to develop new strategies to treat TB and other infectious diseases, leading to the development of new types of medicines to eliminate bacteria. Blocking the action of these essential survival factors, in combination with current antibiotics, has the potential to shorten the time of treatment, increase efficacy against susceptible and drug resistant strains of Mtb, thereby increasing cure rates, and preventing relapse in patients with an impaired inmune system.