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  • Oral presentation
  • Open Access

M. tuberculosis enhances its virulence during replication in blood from HIV patients

  • 1,
  • 1,
  • 2,
  • 3,
  • 2 and
  • 1, 4Email author
BMC Infectious Diseases201414 (Suppl 3) :O12

  • Published:


  • Tuberculosis
  • False Discovery Rate
  • Mycobacterium Tuberculosis
  • Active Infection
  • Iron Acquisition


Mycobacterium tuberculosis and HIV act synergistically to enhance and accelerate the development of tuberculosis and progression of HIV infection to AIDS. Hematogenous dissemination of M. tuberculosis leading to extrapulmonary TB, disseminated TB and miliary TB is greatly increased in HIV+ TB patients. We have compared the transcriptome of M. tuberculosis replicating in whole blood from immunocompetent and immunodeficient individuals to understand how M. tuberculosis adapts to the blood environment during hematogenous dissemination.


Whole genome microarray analysis was performed on RNA from M. tuberculosis replicating in whole blood from PPD negative HIV- healthy donors and HIV+ donors. Genes with a fold change of≥ 2, at a false discovery rate of < 2%, were considered significantly differentially expressed.


M. tuberculosis survives and replicates in blood, and enhances its virulence/pathogenic potential during adaptation to the hematogenous environment. The blood specific transcriptome reflects suppression of dormancy, induction of cell-wall remodeling, alteration in mode of iron acquisition, evasion of immune surveillance and enhanced expression of important virulence factors that drive active infection and dissemination. Compared to replication in HIV blood, these changes are accentuated during replication in blood from HIV patients. The expression of ESAT-6, known to play an important role in dissemination of M. tuberculosis from the lungs, is upregulated in M. tuberculosis growing in blood, and especially dramatically during growth in HIV+ blood.


M. tuberculosis modulates its aggressive progression to disseminated forms of TB by modifying its transcriptome to acquire a phenotype with enhanced virulence that favors active infection and dissemination.

Authors’ Affiliations

Veterans Affairs Medical Center, New York Harbor Health Care System, New York, NY, USA
Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China
Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
New York University Langone Medical Center, Departments of Pathology and Microbiology, New York, NY, USA


© Ryndak et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.