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Background: Several Mycobacterium tuberculosis glycoproteins are involved in tuberculosis pathogenesis. Results: Mycobacterium tuberculosis Rv3242c and Mycobacterium marinum mimG enhance bacillary survival by inhibiting oxidative stress and autophagy pathways in macrophages and zebrafish. Conclusion: Rv3242c and mimG aid intracellular bacterial persistence by modulating host immune responses. Significance: This study has identified a novel virulence factor, which can be considered as drug target for tuberculosis treatment.

This information is current as Survival in Macrophages Autophagy Expression to Enhance Bacterial TLR2-Dependent Cathelicidin and LprE Suppresses Mycobacterium tuberculosis