Abstract
Isoniazid (isonicotinic acid hydrazide, INH) is an effective frontline antituberculosis drug. INH targets several Mycobacterium tuberculosis processes, including mycolic acid biosynthesis, DNA synthesis, and redox potential. M. tuberculosis responds to INH stress by altering the expression level of crucial genes involved in various pathways. In this study, we summarize the induced gene expression pattern of active M. tuberculosis upon INH exposure. Most genes triggered by INH are involved in processes such as mycolic acid biosynthesis, a compensatory response, stress response, and drug efflux. These patterns are absent in dormant M. tuberculosis. The differential INH response pattern can inform future novel measures against M. tuberculosis.
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