Public Health Research Institute, New Jersey Medical School, 225 Warren Street, Newark, NJ 07103, USA.
Tuberculosis (Edinb). 2012 Jan;92(1):60-2. doi: 10.1016/j.tube.2011.09.010. Epub 2011 Oct 20.
Iron acquisition is essential for Mycobacterium tuberculosis (Mtb) virulence. Understanding the molecular mechanisms used by Mtb to scavenge iron during infection might reveal new targets for antimicrobial development. Rv2895c, a homolog of ViuB from Vibrio cholerae has been postulated to be involved in iron-siderophore uptake and utilization in Mtb. This study examines the requirement of Rv2895c for adaptation of Mtb to iron limitation. We show that Rv2895c is dispensable for normal replication of Mtb in iron deficient conditions and in human macrophages. Thus, contrary to the predictions of sequence analysis and in-vitro studies the genetic evidence indicates that in normal conditions Rv2895c is not required for iron acquisition in Mtb.
铁的获取对于结核分枝杆菌（Mtb）的毒力至关重要。了解 Mtb 在感染过程中用于掠夺铁的分子机制可能会揭示出新的抗菌药物开发靶点。Rv2895c 是霍乱弧菌 ViuB 的同源物，据推测它参与了 Mtb 中铁-铁载体的摄取和利用。本研究探讨了 Rv2895c 对 Mtb 适应缺铁条件的需求。我们发现，Rv2895c 在缺铁条件下和人巨噬细胞中对 Mtb 的正常复制是可有可无的。因此，与序列分析和体外研究的预测相反，遗传证据表明，在正常条件下，Rv2895c 不是 Mtb 中铁获取所必需的。
