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

结核病（TB）是影响人类的最古老和最持久的细菌感染性疾病之一。尽管随着疫苗和抗生素的引入，在控制结核病传播方面取得了重大进展，但仍有三分之一的人口受到感染，每年有160万人死亡。抗药性的增加和有效抗生素的有限库存有可能进一步扩大疾病负担。迫切需要新的治疗方法来对抗这种疾病。结核分枝杆菌（Mtb），结核病的病原体，能够挑战我们的免疫系统，并通过逃避我们的自然防御在肺部生存。一般来说，我们的白色血细胞会吞噬和消化微生物来阻止感染，这个过程被称为吞噬作用。然而，结核病产生了一些物质，“生存因子”，停止这一过程，使细菌在白色血细胞内生长和繁殖，然后扩散到附近的细胞。让细菌存活的精确机制仍然知之甚少。我们现在想了解这些生存因素是如何工作的，以及当我们阻止它们的行动时会发生什么。更好地了解这些过程将有助于我们制定治疗结核病和其他传染病的新策略，从而开发出消除细菌的新型药物。阻断这些基本生存因子的作用，与目前的抗生素结合，有可能缩短治疗时间，提高对Mtb易感和耐药菌株的疗效，从而提高治愈率，并预防免疫系统受损患者的复发。

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.