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

The co-evolution of Mycobacterium tuberculosis H37Rv 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 Mycobacterium tuberculosis. Simultaneously, extending the statistical study on Mycobacterium-infected human cord blood CD34+ cells revealed that the human CD34+ genes, S100A8 and FGR (tyrosine-protein kinase, Src2), might be affected in the infection pathogenesis by Mycobacterium. Further, the deduced Mycobacterium-human gene interaction network proposed that mycobacterial coregulators Rv0452 (MarR family regulator) and Rv3862c (WhiB6) triggered genes controlling bacterial metabolism, which influences human immunological pathways involving TLR2 and CXCL8/MAPK8.Communicated by Ramaswamy H. Sarma