Vivek Rao

Senior Scientist
Infectious disease biology

Our lab works on understanding molecular mechanisms that ensue at the host- Mtb interface determine the outcome of infection. Mtb actively invokes a strong type I IFN response to Mtb in host macrophages; underlying mechanisms that govern this response are poorly understood. Type I IFN can regulate the expression of the pro- inflammatory response of macrophages, a key component of the antimycobacterial defense system of host cells. It would be logical to assume that modulation of IFN 1 levels would result in alteration of the antimycobacterial response of macrophages. One of the research focus is to test this hypothesis in cellular and in vivo models of infection. Additionally, we are deciphering the non-coding Mtb directed response network of the host macrophages. We have identified novel lncRNAs that are specifically induced in Mtb infected macrophages. Our efforts would involve testing of the relevance of these noncoding transcripts in cellular models of mycobacterial infections. The current increase in non- pulmonary infections proves the extreme plastic nature of Mtb in terms of adaptation to the host tissues. Neuronal TB accounts for nearly 1% of the TB cases and is one of the most debilitating forms of the infection involving the CNS. We intend to utilize cellular/ animal models for TB infection of the neuronal tissues in order to study various patho-adaptive features of Mtb to the neuronal tissue. Additionally, we are deciphering signatures of Mtb infections in various tissue types by global expression analysis. Unique lipids in its cell wall provide Mtb with a formidable barrier to counter both the host immune effectors and chemical entities. The mechanisms regulating this complex organization is yet not understood fully. By using cutting edge molecular and biochemical techniques, we are actively involved in defining the function of proteins and pathways in mycobacterial physiology and immuno- pathogenesis.
His interests include:

• Type I inteferons play a dominant role in shaping macrophage response to Mtb
• Mtb infections induces novel lncRNA expression that can modulate innate immune responses
• Mtb has evolved novel functions of lipid export and stress survival for membrane trsnporters

Infection with Mtb induces a strong type I IFN response in macrophages; this axis of innate immunity is actively modulated by Mtb stains. Initial events at the host-pathogen interface dictate activation of the type I IFN pathway in macrophages. Novel non coding RNAs that can effectively modulate innate responses have been identified and are being investigated.

Selected Publications:

• Tailored Chemical Properties of 4-Arm Star ShapedPoly(d,l-lactide) as Cell Adhesive Three-Dimensional Scaffolds. Balavigneswaran CK, Mahto SK, Subia B, Prabhakar A, Mitra K, Rao V, Ganguli M,Ray B, Maiti P, Misra N. Bioconjug Chem.2017 Apr 19;28(4):1236-1250. doi: 10.1021/acs.bioconjchem.7b00071.
• Expression profiling of lymph nodes in tuberculosis patients reveal inflammatory milieu at site of infection. Maji A, Misra R, Kumar Mondal A, Kumar D, Bajaj D, Singhal A, Arora G, BhaduriA, Sajid A, Bhatia S, Singh S, Singh H, Rao V, Dash D, Baby Shalini E, SarojiniMichael J, Chaudhary A, Gokhale RS, Singh Y. SciRep. 2015 Oct 15;5:15214. doi: 10.1038/srep15214.
• Integration host factor of Mycobacterium tuberculosis, mIHF, compactsDNA by a bending mechanism. Mishra A, Vij M, Kumar D, Taneja V, Mondal AK, Bothra A, Rao V, Ganguli M,Taneja B.
  PLoS One. 2013 Jul 26;8(7):e69985. doi:10.1371/journal.pone.0069985.
• Redundant function of cmaA2 andmmaA2 in Mycobacterium tuberculosis cis cyclopropanation of oxygenated mycolates. Barkan D, Rao V, Sukenick GD, Glickman MS. J Bacteriol. 2010 Jul;192(14):3661-8. doi: 10.1128/JB.00312-10.
• Trans-cyclopropanation ofmycolic acids on trehalose dimycolate suppresses Mycobacterium tuberculosis-induced inflammation and virulence. Rao V, Gao F, Chen B, Jacobs WR Jr, Glickman MS. J Clin Invest. 2006 Jun;116(6):1660-7.