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Despite considerable progress in understanding the pathogenesis of  Mycobacterium tuberculosis  ( Mtb ), development of new therapeutics and vaccines against it has proven difficult. This is at least in part due to the use of less than optimal models of  in-vivo Mtb  infection, which has precluded a study of the physiology of the pathogen in niches where it actually persists. C3HeB/FeJ (Kramnik) mice develop human-like lesions when experimentally infected with  Mtb  and thus make available, a faithful and highly tractable system to study the physiology of the pathogen  in-vivo . We compared the transcriptomics of  Mtb  and various mutants in the DosR (DevR) regulon derived from Kramnik mouse granulomas to those cultured  in-vitro . We recently showed that mutant Δ dosS  is attenuated in C3HeB/FeJ mice. Aerosol exposure of mice with the mutant mycobacteria resulted in a substantially different and a relatively weaker transcriptional response (< = 20 genes were induced) for the functional category ‘Information Pathways’ in  Mtb :Δ dosR ; ‘Lipid Metabolism’ in  Mtb :Δ dosT ; ‘Virulence, Detoxification, Adaptation’ in both  Mtb :Δ dosR  and  Mtb :Δ dosT ; and ‘PE/PPE’ family in all mutant strains compare to wild-type  Mtb  H37Rv, suggesting that the inability to induce DosR functions to different levels can modulate the interaction of the pathogen with the host. The  Mtb  genes expressed during growth in C3HeB/FeJ mice appear to reflect adaptation to differential nutrient utilization for survival in mouse lungs. The genes such as  glnB , Rv0744c, Rv3281,  sdhD/B ,  mce4A ,  dctA  etc. downregulated in mutant Δ dosS  indicate their requirement for bacterial growth and flow of carbon/energy source from host cells. We conclude that genes expressed in  Mtb  during  in-vivo  chronic phase of infection in Kramnik mice mainly contribute to growth, cell wall processes, lipid metabolism, and virulence.

In-Vivo Gene Signatures of Mycobacterium tuberculosis in C3HeB/FeJ Mice