Metabolomics and stable isotope labelling studies of virulent Mycobacterium tuberculosis reveal a de-centralised metabolic network able to utilise various amino acids as nitrogen sources to a better extent than ammonium.
A humanized transgenic mouse model reveals that CD1b-restricted, mycolic acid-specific T cells play a protective role during Mycobacterium tuberculosis infection.
An unbiased forward genetic screen identified genes in Mycobacterium tuberculosis that are required for fatty acid import when the bacterium is residing within macrophages.
Cryo-electron microscopy structures show how the clinically used antimicrobial fidaxomicin binds and inhibits Mycobacterium tuberculosis RNA polymerase by acting like a doorstop to jam the enzyme in an open conformation via the general transcription factor RbpA.
Intrinsic tolerance of Mycobacterium tuberculosis toward the world's most successful antibacterials, β-lactams, is dependent on cytoplasmic redox potential and an intracellular redox-sensor WhiB4.
SatS of Mycobacterium tuberculosis is a new protein export chaperone with a role in exporting proteins by the specialized SecA2 pathway and a role in intracellular growth in macrophages.
The rapid killing of macrophages by Mycobacterium tuberculosis aggregates, and the subsequent proliferation of the bacteria inside the dead cell, leads to a cell death cascade and explains the coupling of necrosis and pathogen growth observed in active disease.
Inflammatory monocytes carry live Mycobacteria from the lung to draining lymph nodes and acquire many characteristics of dendritic cells but fail to stimulate proliferation of CD4 T cells.
