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Comment
. 2017 Apr 28:8:466.
doi: 10.3389/fimmu.2017.00466. eCollection 2017.

Commentary: Modification of Host Responses by Mycobacteria

Ashutosh Kumar  1 , Mamta Rani  2 , Nasreen Z Ehtesham  3 , Seyed E Hasnain  1   4   5
Affiliations
Comment

Commentary: Modification of Host Responses by Mycobacteria

Ashutosh Kumar et al. Front Immunol. .
No abstract available

Keywords: Mycobacterium tuberculosis; host pathways; persisters; stress adaptation; virulence factors.

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Figures

Figure 1
Figure 1
Growth regulation by Mycobacterium for adaptation to stress/dormancy. Mycobacterium tuberculosis (M.tb) IciA (inhibitor of chromosome initiation) binds to the A + T rich oriC region of the M.tb genome and inhibits helix opening resulting in the arrest of chromosomal DNA replication (31). Activated toxin–antitoxin (TA) systems cleave mRNA to shut down metabolic activity (32). Peddireddy et al. (35) have also described the role of TA systems in M.tb and Mycobacterium smegmatis to remain in non-replicating phase that help bacteria in antibiotic tolerance. Highly expressed protein DATIN/RafH of Mycobacterium inhibits translation by binding with the ribosome under conditions of stress (33, 34). Confirmed and putative roles are indicated with continuous and dashed arrows, respectively.
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