Mycobacterium tuberculosis (Mtb) characteristically causes an asymptomatic infection. While this latent tuberculosis infection (LTBI) is not contagious, reactivation to active tuberculosis disease (TB) causes the patient to become infectious. A vaccine has existed for TB for a century, while drug treatments have been available for over 70 years; despite this, TB remains a major global health crisis. Understanding the factors which allow the bacillus to control responses to host stress and mechanisms leading to latency are critical for persistence. Similarly, molecular switches which respond to reactivation are important. Recently, research in the field has sought to focus on reactivation, employing system-wide approaches and animal models. Here, we describe the current work that has been done to elucidate the mechanisms of reactivation and stop reactivation in its tracks.

结核分枝杆菌（结核杆菌）通常会导致无症状感染。虽然这种潜伏性结核感染（LTBI）不具传染性，但重新激活为活动性结核病（TB）会使患者具有传染性。结核病疫苗已有一个世纪的历史了，而药物治疗已有70多年的历史了。尽管如此，结核病仍然是全球主要的健康危机。了解允许细菌控制宿主应激反应的因素和导致潜伏期的机制对于持久性至关重要。类似地，响应于再活化的分子开关也很重要。最近，该领域的研究试图利用系统范围的方法和动物模型将精力集中在重新激活上。在这里，我们描述了为阐明重新激活机制并停止其轨道中的重新激活而进行的当前工作。