Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), which claims 
approximately two million people annually, remains a global health concern. The 
non-replicating or dormancy like state of this pathogen which is impervious to 
anti-tuberculosis drugs is widely recognized as the culprit for this scenario. 
The dormancy survival regulator (DosR) regulon, composed of 48 co-regulated 
genes, is held as essential for Mtb persistence. The DosR regulon is regulated 
by a two-component regulatory system consisting of two sensor kinases-DosS 
(Rv3132c) and DosT (Rv2027c), and a response regulator DosR (Rv3133c). The 
underlying regulatory mechanism of DosR regulon expression is very complex. Many 
factors are involved, particularly the oxygen tension. The DosR regulon enables 
the pathogen to persist during lengthy hypoxia. Comparative genomic analysis 
demonstrated that the DosR regulon is widely distributed among the mycobacterial 
genomes, ranging from the pathogenic strains to the environmental strains. 
In-depth studies on the DosR response should provide insights into its role in 
TB latency in vivo and shape new measures to combat this exceeding recalcitrant 
pathogen.