Mycobacterium tuberculosis is the causative agent of tuberculosis disease, which has developed a myriad of exceptional features contributing to its survival within the hostile environment of host cell. Unique cell wall structure with high lipid content plays an imperative role in the pathogenicity of mycobacteria. Cell wall components of MTB such as lipoarabinomannan and Trehalose dimycolate (cord factor) are virulent in nature apart from its virulence genes. Virulent effect of these factors on host cells reduces host cell immunity. LAM has been known to inhibit phagosome maturation by inhibiting the Ca2+/calmodulin phosphatidyl inositol-3-kinase hvps34 pathways. Moreover, TDM (Trehalose dimycolate) also inhibits fusion between phospholipid vesicles and migration of polymorphonuclear neutrophils. The objective of this paper is to understand the virulence of LAM and cord factor on host cell which might be helpful to design an effective drug against tuberculosis. 1. Introduction Mycobacterium tuberculosis (MTB) is exceptionally successful pathogen with unique characteristic features which make it highly pathogenic [1]. Cell wall of MTB is composed of 60% of lipids. Major fraction of its cell wall is mycolic acid, Cord factor, and Wax-D [2, 3]. The cell wall of MTB is composed of two segments: outer part and core of cell wall (Figure 1). Core of cell wall is made up of peptidoglycan (PG), covalently attached with arabinogalactan (AG) and mycolic acids subsequently, forming the mycolyl arabinogalactan-peptidoglycan (mAGP) complex. Upper part is composed of free lipids which are linked with fatty acids. Mostly this part is made up of different cell wall proteins, the phosphatidylinositol mannosides (PIMs), Lipomannan (LM), and Lipoarabinomannan (LAM). These proteins along with lipids and glycoconjugate lipids act as effector molecules of signaling process, and the insoluble core is essential for the viability of the cell [3]. LAM blocks phagosomal maturation in host cell either by blocking the trafficking pathway from trans-Golgi network (TGN) to phagosomes which itself depends on early endosomal autoantigen 1 (EEA1), an essential Rab5 factor recruitment to early phagosomes, or by inhibiting the Ca2+ concentration in macrophages, as Ca2+ is an essential factor for phagosomal maturation [4]. Another virulence factor, produced by MTB, is Cord factor. Cord factor behaves differentially according to its localization. It is nontoxic, when present on organisms and protects them from macrophage destruction, but it becomes toxic on lipid surfaces. TDM inhibits the
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