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Clinical and Developmental Immunology
Volume 2011, Article ID 980594, 9 pages
Review Article

Changing Concepts of “Latent Tuberculosis Infection” in Patients Living with HIV Infection

1The Desmond Tutu HIV Centre, Institute for Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Anzio Road, Observatory 7925, Cape Town, South Africa
2Clinical Research Unit, Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London WC1E 7HT, UK
3Clinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine and Department of Medicine, Faculty of Health Sciences, University of Cape Town, Observatory 7925, South Africa
4Division of Mycobacterial Research, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK
5Division of Medicine, Imperial College London, London W2 1PG, UK

Received 9 June 2010; Accepted 25 August 2010

Academic Editor: Estee Torok

Copyright © 2011 Stephen D. Lawn et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


One third of the world’s population is estimated to be infected with Mycobacterium tuberculosis, representing a huge reservoir of potential tuberculosis (TB) disease. Risk of progression to active TB is highest in those with HIV coinfection. However, the nature of the host-pathogen relationship in those with “latent TB infection” and how this is affected by HIV coinfection are poorly understood. The traditional paradigm that distinguishes latent infection from active TB as distinct compartmentalised states is overly simplistic. Instead the host-pathogen relationship in “latent TB infection” is likely to represent a spectrum of immune responses, mycobacterial metabolic activity, and bacillary numbers. We propose that the impact of HIV infection might better be conceptualised as a shift of the spectrum towards poor immune control, higher mycobacterial metabolic activity, and greater organism load, with subsequent increased risk of progression to active disease. Here we discuss the evidence for such a model and the implications for interventions to control the HIV-associated TB epidemic.