Role of the Dihydrofolate Reductase DfrA (Rv2763c) in Trimethoprim-Sulfamethoxazole (Co-Trimoxazole) Resistance in Mycobacterium tuberculosis | Zendy

Claudio U. Köser | Zendy; David Summers | Zendy; John A. C. Archer | Zendy

Open Access

Role of the Dihydrofolate Reductase DfrA (Rv2763c) in Trimethoprim-Sulfamethoxazole (Co-Trimoxazole) Resistance in Mycobacterium tuberculosis

Author(s) -

Claudio U. Köser,

David Summers,

John A. C. Archer

Publication year - 2010

Publication title -

antimicrobial agents and chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.07

H-Index - 259

eISSN - 1070-6283

pISSN - 0066-4804

DOI - 10.1128/aac.00876-10

Subject(s) - dihydrofolate reductase , mycobacterium tuberculosis , trimethoprim , sulfamethoxazole , isoniazid , point mutation , genetics , microbiology and biotechnology , mutation , tuberculosis , biology , antibiotics , medicine , gene , pathology

We thank Wang et al. for clarifying the role of the dihydrofolate reductase DfrA (Rv2763c) in isoniazid (INH) resistance ([16][1]). Concerning potential candidates for the unknown INH resistance mechanism(s), we would like to point out that the aldC ( Rv2858c ) T21A mutation is also present in

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