Thirty years ago Stanley Falkow formulated molecular Koch's postulates as a framework to help dissect the contribution of microbial genes to their pathogenicity (Box 1). Three years later, his advice led me to develop Mycobacterium marinum, a close genetic relative of Mycobacterium tuberculosis, as a model for tuberculosis pathogenesis. Here, I discuss insights into M. tuberculosis pathogenicity from studying M. marinum in the zebrafish, and frame them in terms of molecular Koch's postulates. The highly orchestrated life cycle of M. tuberculosis is achieved in substantial measure not by "traditional" pathogen-exclusive virulence genes acquired along its evolutionary history, but rather by genes that are shared with its environmental ancestors. Together, these genes support its tactics of subterfuge and exploitation to overcome host immunity so as to produce the transmissible disease that ensures the evolutionary survival of this obligate human pathogen.

中文翻译：

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通过分子科赫假说的镜头可以看到结核分枝杆菌的致病性。

三十年前，斯坦利·福尔科夫（Stanley Falkow）将分子科赫的假设作为框架来帮助剖析微生物基因对其致病性的贡献（专栏1）。三年后，他的建议促使我开发了结核分枝杆菌的近亲亲戚-海洋分枝杆菌，作为结核病发病机制的模型。在这里，我将通过研究斑马鱼中的海藻分枝杆菌来讨论结核分枝杆菌致病性的见解，并根据分子的科赫假设来构架它们。结核分枝杆菌的高度协调的生命周期在很大程度上不是通过沿其进化史获得的“传统”病原体专有毒力基因来实现，而是通过与其环境祖先共享的基因来实现。一起，