LAXMAN S MEENA
Articles written in Journal of Biosciences
Volume 43 Issue 1 March 2018 pp 149-154 Mini-Review
The ability of Mycobacterium tuberculosis (M. tuberculosis) to accumulate lipid-rich molecules as an energy sourceobtained from host cell debris remains interesting. Additionally, the potential of M. tuberculosis to survive under differentstress conditions leading to its dormant state in pathogenesis remains elusive. The exact mechanism by which these lipidbodies generated in M. tuberculosis infection and utilized by bacilli inside infected macrophage for its survival is still notunderstood. In this, during bacillary infection, many metabolic pathways are involved that influence the survival of M.tuberculosis for their own support. However, the exact energy source derived from infecting host cells remain elusive.Therefore, this study highlights several alternative energy sources in the form of triacylglycerol (TAG) and fatty acids, i.e.oleic acids accumulation, which are essential in dormancy-like state under M. tuberculosis infection. The prominent stage intuberculosis (TB) infection is re-establishment of M. tuberculosis under stress conditions and deployment of a confinedstrategy to utilize these biomolecules for its persistence survival. So, growing in our understanding of these pathways willhelp us in accelerating therapies, which could reduce TB prevalence world widely.
Volume 44 Issue 1 March 2019 Article ID 0024 Review
In today’s era tuberculosis is a major threat to human population. The lethality of this disease is caused by very efficientlythrived bacteria Mycobacterium tuberculosis (M. tuberculosis). Ca2? plays crucial role in maintenance of cellular homeostasis.Bacilli survival in human alveolar macrophages majorly depends on disruption in Ca2? signaling. Bacilli sustainabilityin phagosome lies in the interruption of phagolysosomal fusion, which is possible because of low intracellularCa2? concentration. Bacilli contain various Ca2? binding proteins which help in regulation of Ca2? signaling for its ownbenefit. For the survival of pathogen, it requires alteration in normal Ca2? concentration in healthy cell. In this review weaim to find the various Ca2? binding domains which are present in several Ca2? binding proteins of M. tuberculosis andvariety of roles played by Ca2? to survive bacilli within host cell. This manuscript emphasizes the Ca2? binding domainspresent in PE_PGRS group of gene family and their functionality in M. tuberculosis survival and pathogenesis.
Volume 46, 2020
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