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Oxidative damage and delayed replication allow viable Mycobacterium tuberculosis to go undetected

ABSTRACT: Oxidative damage and delayed replication allow viable Mycobacterium tuberculosis to go undetected

PROVIDER: PRJNA748428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15202800_1.fastq.gz	Fastqsanger.gz
	SRR15202800_2.fastq.gz	Fastqsanger.gz
	SRR15202801_1.fastq.gz	Fastqsanger.gz
	SRR15202801_2.fastq.gz	Fastqsanger.gz
	SRR15202802_1.fastq.gz	Fastqsanger.gz

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Project description:“Viable but nonculturable” states of bacteria pose challenges for environmental and clinical microbiology, but their biological mechanisms remain obscure. Mycobacterium tuberculosis (Mtb), the leading cause of death from infection until the coronavirus disease 2019 pandemic, affords a notable example of this phenotype. Mtb can enter into a “differentially detectable” (DD) state associated with phenotypic antimicrobial resistance. In this state, Mtb cells are viable but undetectable as colony-forming units. We found that Mtb cells enter the DD state when they undergo sublethal oxidative stress that damages their DNA, proteins, and lipids. In addition, their replication process is delayed, allowing time for repair. Mycobacterium bovis and its derivative, BCG, fail to enter the DD state under similar conditions. These findings have implications for tuberculosis latency, detection, relapse, treatment monitoring, and development of regimens that overcome phenotypic antimicrobial resistance.

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