Deletion of pknG Abates Reactivation of Latent Mycobacterium tuberculosis in Mice

Abstract

Eradication of tuberculosis (TB), caused by Mycobacterium tuberculosis ( Mtb ), has been a challenge due to its uncanny ability to survive in a dormant state inside host granulomas for decades. Mtb rewires its metabolic and redox regulatory networks to survive in the hostile hypoxic and nutrient-limiting environment, facilitating the formation of drug-tolerant persisters. Previously, we showed that protein kinase G (PknG), a virulence factor required for lysosomal escape, aids in metabolic adaptation, thereby promoting the survival of nonreplicating mycobacteria.