Attenuation ofMycobacterium tuberculosisFunctionally Disrupted in a Fatty Acyl–Coenzyme A Synthetase GenefadD5

摘要: One key adaptation that Mycobacterium tuberculosis established to survive long term in vivo is a reliance on lipids as an energy source. M. H37Rv has 36 fadD genes annotated putative fatty acyl-CoA synthetase genes, which encode enzymes activate acids for metabolism. such gene, fadD5 (Rv0166), located within the mce1 operon, cluster of associated with persistence. We disrupted acid binding site tuberculosis. No significant differences were found growth mutant and wild-type strains vitro nutrient-rich broth or activated RAW264.7 cells. However, was diminished minimal medium containing mycolic acid, but not other long-chain acids. C57BL/6 mice infected survived significantly longer than those wild-type, never attained plateau phase infection mouse lungs. The steady-state maintained up 168 days at level one two logs less shown by wild-type. These observations raise rather intriguing possibility FadD5 may serve recycle long-term survival tubercle bacilli.