Albert Einstein College of Medicine, Department of Microbiology and Immunology, 1300 Morris Park Ave., Bronx, NY 10461, USA.
Antimicrob Agents Chemother. 2011 Sep;55(9):4422-3. doi: 10.1128/AAC.00564-11. Epub 2011 Jun 27.
A search to identify new mechanisms of isoniazid resistance in Mycobacterium bovis led to the isolation of mutants defective in mycothiol biosynthesis due to mutations in genes coding for the glycosyltransferase (mshA) or the cysteine ligase (mshC). These mutants showed low-level resistance to isoniazid but were highly resistant to ethionamide. This study further illustrates that mutations in mycothiol biosynthesis genes may contribute to isoniazid or ethionamide resistance across mycobacterial species.
一项旨在确定结核分枝杆菌异烟肼耐药新机制的研究导致了由于编码糖基转移酶(mshA)或半胱氨酸连接酶(mshC)的基因突变而导致分枝菌酸生物合成缺陷的突变体的分离。这些突变体对异烟肼表现出低水平的耐药性,但对乙硫异烟胺高度耐药。本研究进一步表明,分枝菌酸生物合成基因的突变可能导致结核分枝杆菌和非结核分枝杆菌对异烟肼或乙硫异烟胺的耐药。