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[Seminar] Mycobacteria-HIV coalition: the cellular events behind the emerging threat

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Sharmistha Banerjee, School of Life Sciences, University of Hyderabad, India

When 20 Dec, 2016 from
10:00 am to 11:00 am
Where Auditorium
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Seminar

Title: Mycobacteria-HIV coalition: the cellular events behind the emerging threat

Speaker: Sharmistha Banerjee

Affiliation: Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad, Telangana State, India

 

Abstract:

Mycobacterium tuberculosis complex comprises of phylogenetically close groups of Mycobacterium species that infect humans causing tuberculosis (TB), a disease which despite being curable, has re-emerged as a global pandemic. Multiple factors, including lack of effective vaccine, failure of early detection, emergence of drug resistance and, of late, the co-epidemics with HIV/AIDS, have limited the success of TB disease management. TB is predominantly caused by pathogenic mycobacteria, Mycobacterium tuberculosis (M. tb), however non-pathogenic and attenuated strains of mycobacteria establish infection asymptomatically in HIV patients even before T-cell depletion is apparent. These environmental mycobacteria, highly prevalent in natural and artificial (including chlorinated municipal water) niches, are emerging as new threat to human health, especially to HIV infected population, resulting in an increased risk of disease progression from both the pathogens in the individuals concurrently infected with mycobacteria and HIV as compared to those carrying single infections. These seemingly harmless non-pathogenic mycobacteria, that are otherwise cleared, establish as opportunistic infections adding to HIV associated complications, re-emergence of latent infections and drug resistant mycobacterial strains. Though immune-evading strategies of pathogenic mycobacteria are known, the mechanisms underlying the early events by which opportunistic mycobacteria establish infection in macrophages influencing HIV infection are unclear. We undertook a comparative proteomics approach to understand the same and identified differential distribution of 260 host and 92 pathogenic proteins in phagosome-enriched fractions from Mycobacteria mono- and HIV-Mycobacteria co-infected THP-1 cells by LC-MALDI-MS/MS, suggesting the perturbed pathways responsible for this synergism. Some of recent findings from the lab will be shared.

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