Journal
TRENDS IN MICROBIOLOGY
Volume 28, Issue 10, Pages 832-850Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.tim.2020.04.010
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Funding
- Washington University in St Louis
- National Institutes of Health (NIH) [R01 HL105427, R01 AI134236, R01 AI111914, R01 AI123780]
- NIH Training grant [T32 HL007317-41]
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Over a quarter of the world's population is infected with Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB). Approximately 3.4% of new and 18% of recurrent cases of TB are multidrug-resistant (MDR) or rifampicin-resistant. Recent evidence has shown that certain drug-resistant strains of Mtb modulate host metabolic reprogramming, and therefore immune responses, during infection. However, it remains unclear how widespread these mechanisms are among circulating MDR Mtb strains and what impact drug-resistance-conferring mutations have on immunometabolism during TB. While few studies have directly addressed metabolic reprogramming in the context of drug-resistant Mtb infection, previous literature examining how drug-resistance mutations alter Mtb physiology and differences in the immune response to drug-resistant Mtb provides significant insights into how drug-resistant strains of Mtb differentially impact immunometabolism.
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