Ph.D, INSERM-UPMC, Paris
Tuberculosis (TB) is a disease caused by the bacteria Mycobacterium tuberculosis.Tuberculosis claims about 2 million lives annuallyand is the leading cause of death worldwide due to a single bacterial agent. The situation is particularly alarming in several developing countries including India, with India accounting for 30% of the global burden of tuberculosis. In addition, the emergence and spread of drug resistant strains (that are resistant to most antibiotics currently in use)and thesynergistic association of this disease with AIDS, are posing major challenges for tuberculosis control. For these reasons, world health organisation (WHO) has announced tuberculosis as a ‘global emergency’.
Mycobacteria are intra-cellular pathogens that have developed specific mechanisms to invade and survive within their host. The host-pathogen interplay is complex. Upon infection with M. tuberculosis, only about 10% of the infected population develop highly contagious, active tuberculosis disease. The rest of the population exhibit a clinically latent infection characterized by the persistence of possibly dormant bacilli. In latently infected individuals the infection may reactivate and cause active tuberculosis. The reactivation risk is higher when confronted by immune suppression, for example, upon co-infection with HIV.
M. tuberculosis poses extraordinaryintellectual and medical challenge, as ~40% of its genes are of unknownfunction. The entire genome of M. tuberculosis, comprising approximately 3924 open reading frames, has been sequenced. Examining the mechanisms by which M. tuberculosis activates or evades the host immune responses is a key to developing a greater understanding of the pathology of tuberculosis. In this context, our research interests focus on: understanding the host-pathogen interaction in tuberculosis at molecular level and gaining insights into the immune surveillance mechanisms of the host during infection, with an ultimate aim of designing better diagnosis and intervention strategies for tuberculosis.
We are specifically interested in
(i) Identifying and characterizing novel genes that contribute to the virulence and pathogenicity of M.tuberculosis
(ii) Understanding the role of novel innate immune receptors in modulating immune responses
(iii) Role of B cells in immune response to tuberculosis
- Vani J, Shaila MS, Trinath J, Balaji KN, Kaveri SV, Bayry J. Cell wall-associated Rv3812 protein of Mycobacterium tuberculosis induces strong dendritic cell-mediated IFNγ responses and exhibits vaccine potential. J Infect Dis. 2013, 208(6):1034-6
- Vani J, Sharma M, Shaila MS, Kaveri SV, Bayry J. Effect of gp120 on dendritic cell-derived chemokines: relevance for the efficacy of gp120-based vaccines for HIV-1. Clin Vaccine Immunol.2012, 19(8):1335-6.
- Vani J, Shaila MS, Rao MKN, Krishnaswamy UM, Kaveri SV and Bayry J. 2009. B lymphocytes from tuberculosis patients exhibit hampered antigen-specific responses with a concomitant over-expression of IL-8. J Infect Dis. 2009, 200(3): 481-2
- Vani J, Bansal K, Kazatchkine MD, Kaveri SV, Bayry J, Immuno intervention for patients with HIV and tuberculosis. Lancet Infect Dis. 2009, 9(6):332-3
- Vani J, Nayak R, Shaila MS. Maintenance of antigen-specific immunological memory through variable regions of heavy and light chains of anti-idiotypic antibody.Immunology.2007,120(4):486-96.