ArticlePloS one2014
Transcriptional profiling of Mycobacterium tuberculosis replicating ex vivo in blood from HIV- and HIV+ subjects.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Genome-wide transcriptional landscape ofFrontiers in immunology · 2026Article
- Application of metagenomic next-generation sequencing in HIV-negative hematogenous disseminated tuberculosis.Frontiers in cellular and infection microbiology · 2026Article
- Transcriptional response to the host cell environment of a multidrug-resistant Mycobacterium tuberculosis clonal outbreak Beijing strain reveals its pathogenic features.Scientific reports · 2021Article
- A Low-Prevalence Single-Nucleotide Polymorphism in the Sensor Kinase PhoR inFrontiers in microbiology · 2021Article
- Up regulated virulence genes in M. tuberculosis H37Rv gleaned from genome wide expression profiles.Bioinformation · 2021Article
- Review
- Transcriptome analysis of mycobacteria in sputum samples of pulmonary tuberculosis patients.PloS one · 2017Article
- Transcriptional Profiling ofGenomics data · 2015Article
- A comprehensive map of genome-wide gene regulation in Mycobacterium tuberculosis.Scientific data · 2015Article
- Transcriptional profile of Mycobacterium tuberculosis replicating in type II alveolar epithelial cells.PloS one · 2015Article
- The transition from iron starvation to iron sufficiency as an important step in the progression of infection.Science progress · 2014Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Hematogenous dissemination of Mycobacterium tuberculosis (M. tb) occurs during both primary and reactivated tuberculosis (TB). Although hematogenous dissemination occurs in non-HIV TB patients, in ∼80% of these patients, TB manifests exclusively as pulmonary disease. In contrast, extrapulmonary, disseminated, and/or miliary TB is seen in 60-70% of HIV-infected TB patients, suggesting that hematogenous dissemination is likely more common in HIV+ patients. To understand M. tb adaptation to the blood environment during bacteremia, we have studied the transcriptome of M. tb replicating in human whole blood. To investigate if M. tb discriminates between the hematogenous environments of immunocompetent and immunodeficient individuals, we compared the M. tb transcriptional profiles during replication in blood from HIV- and HIV+ donors. Our results demonstrate that M. tb survives and replicates in blood from both HIV- and HIV+ donors and enhances its virulence/pathogenic potential in the hematogenous environment. The M. tb blood-specific transcriptome reflects suppression of dormancy, induction of cell-wall remodeling, alteration in mode of iron acquisition, potential evasion of immune surveillance, and enhanced expression of important virulence factors that drive active M. tb infection and dissemination. These changes are accentuated during bacterial replication in blood from HIV+ patients. Furthermore, the expression of ESAT-6, which participates in dissemination of M. tb from the lungs, is upregulated in M. tb growing in blood, especially during growth in blood from HIV+ patients. Preliminary experiments also demonstrate that ESAT-6 promotes HIV replication in U1 cells. These studies provide evidence, for the first time, that during bacteremia, M. tb can adapt to the blood environment by modifying its transcriptome in a manner indicative of an enhanced-virulence phenotype that favors active infection. Additionally, transcriptional modifications in HIV+ blood may further accentuate M. tb virulence and drive both M. tb and HIV infection.
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Registered trials
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