A systematic computational analysis of <i>Mycobacterium tuberculosis H37Rv</i> and human CD34+ genomic expression reveals crucial molecular entities involved in infection progression

The co-evolution of <i>Mycobacterium tuberculosis H37Rv</i> along with its host systems enables the pathogenic bacterium to emerge as a multi-drug resistant form. This creates challenges for a more efficacious treatment strategy that can mitigate the infection. Working towards the same, our study followed a mathematical and statistical approach proposing that mycobacterial transcription factors regulating virulence and adaptation, host cell cytoplasmic component metabolism, oxidoreductase activity and respiratory ETC would be targets for antibiotics against <i>Mycobacterium tuberculosis.</i> Simultaneously, extending the statistical study on <i>Mycobacterium-</i>infected human cord blood CD34+ cells revealed that the human CD34+ genes, <i>S100A8</i> and <i>FGR</i> (tyrosine-protein kinase, Src2), might be affected in the infection pathogenesis by <i>Mycobacterium</i>. Further, the deduced <i>Mycobacterium-</i>human gene interaction network proposed that mycobacterial coregulators <i>Rv0452</i> (MarR family regulator) and <i>Rv3862c</i> (WhiB6) triggered genes controlling bacterial metabolism, which influences human immunological pathways involving TLR2 and CXCL8/MAPK8. Communicated by Ramaswamy H. Sarma