Exogenous Reinfection with Multidrug-Resistant Mycobacterium tuberculosis in Patients with Advanced HIV Infection

Small, Peter M.; Shafer, Robert W.; Hopewell, Philip C.; Singh, Samir P.; Murphy, Mary; Desmond, Ed; Sierra, Marcelino F.; Schoolnik, Gary K.

doi:10.1056/nejm199304223281601

Cited by 442 publications

(204 citation statements)

References 21 publications

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“…The reinfection of patients previously treated for tuberculosis also challenges the notion that prior exposure to M. tuberculosis induces protective immunity (7,(43)(44)(45). Clearly, delineating how memory T cells develop during M. tuberculosis infection, defining which memory T cell subsets are critical for the control of infection, and understanding how the latent phase of the infection affects the maintenance of memory T cells are all important goals if we are to develop an effective vaccine against tuberculosis.…”

Section: Discussionmentioning

confidence: 99%

“…Briefly, ELISPOT plates were coated with capture IFN-␥ Ab overnight at 4°C and blocked with complete medium for 2 h at room temperature. CD8 ϩ T cells purified from individual infected spleens or lungs by positive selection using CD8␣ immunomagnetic beads and MACS LS ϩ columns, as per manufacturer's protocol (Miltenyi Biotec), were stimulated in triplicate with TB10.3/10.4 20 -28 peptide and irradiated naive splenocytes for 40 -44 h at 37°C (7). In all experiments, the purity of CD8 ϩ cells was Ͼ90%, as determined by flow cytometry.…”

Section: Elispot Assay For Ifn-␥mentioning

confidence: 99%

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Antigen-Specific CD8+ T Cells and the Development of Central Memory during Mycobacterium tuberculosis Infection

Kamath

Woodworth

Behar

2006

The Journal of Immunology

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Whether true memory T cells develop in the face of chronic infection such as tuberculosis remains controversial. To address this question, we studied CD8+ T cells specific for the Mycobacterium tuberculosis ESAT6-related Ags TB10.3 and TB10.4. The shared epitope TB10.3/10.420–28 is presented by H-2 Kd, and 20–30% of the CD8+ T cells in the lungs of chronically infected mice are specific for this Ag following respiratory infection with M. tuberculosis. These TB10.3/10.420–28-specific CD8+ T cells produce IFN-γ and TNF and express CD107 on their cell surface, which indicates their likely role as CTL in vivo. Nearly all of the Ag-specific CD8+ T cells in the lungs of chronically infected mice had a T effector cell phenotype based on their low expression of CD62L and CD45RB. In contrast, a population of TB10.3/10.420–28-specific CD8+ T cells was identified in the lymphoid organs that express high levels of CD62L and CD45RB. Antibiotic treatment to resolve the infection led to a contraction of the Ag-specific CD8+ T cell population and was accompanied by an increase in the proportion of CD8+ T cells with a central memory phenotype. Finally, challenge of memory-immune mice with M. tuberculosis was accompanied by significant expansion of TB10.3/10.420–28-specific CD8+ T cells, which suggests that these cells are in fact functional memory T cells.

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Section: Discussionmentioning

confidence: 99%

Section: Elispot Assay For Ifn-␥mentioning

confidence: 99%

Antigen-Specific CD8+ T Cells and the Development of Central Memory during Mycobacterium tuberculosis Infection

Kamath

Woodworth

Behar

2006

The Journal of Immunology

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“…Nowhere has this approach been used more rigorously than in the pioneering work on the molecular epidemiology of tuberculosis (TB). Since the development of standardized methods for DNA fingerprinting of Mycobacterium tuberculosis, molecular techniques have been used to estimate the fraction of cases attributable to recent transmission of M. tuberculosis (7)(8)(9)(10)(11)(12)(13)(14), identify host-specific risk factors for disease spread (15)(16)(17)(18), document exogenous reinfection (19)(20)(21), and study patterns of drug resistance (22)(23)(24). Investigators also have begun to use these methods to explore potential strain-specific differences in bacterial phenotypes such as tissue tropism, virulence, and transmissibility (25,26).…”

mentioning

confidence: 99%

Determinants of cluster distribution in the molecular epidemiology of tuberculosis

Murray

2002

Proc. Natl. Acad. Sci. U.S.A.

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Recently developed molecular techniques have revolutionized the epidemiology of tuberculosis. Multiple studies have used these tools to examine the population structure of Mycobacterium tuberculosis isolates in different communities. The distributions of clusters of M. tuberculosis isolates in these settings may variously reflect social mixing patterns or the differential fitness of specific clones of the organism. We developed an individual-based microsimulation of tuberculosis transmission to explore social and demographic determinants of cluster distribution and to observe the effect of transmission dynamics on the empiric data from molecular epidemiologic studies. Our results demonstrate that multiple hostrelated factors contribute to wide variation in cluster distributions even when all strains of the organism are assumed to be equally transmissible. These host characteristics include interventions such as chemotherapy, vaccination and chemoprophylaxis, HIV prevalence, the age structure of the population, and the prevalence of latent tuberculosis infection. We consider the implications of these results for the interpretation of cluster studies of M. tuberculosis as well as the more general application of microsimulation models to infectious disease epidemiology.O ver the past 10 years, molecular tools have become available that have changed the way that epidemiologists study the transmission of infectious disease (1). In addition to their role in detecting unsuspected transmission links (2-4), molecular markers are increasingly being used to study transmission patterns within populations and to evaluate host-and strain-specific risk factors for disease spread (5, 6). Nowhere has this approach been used more rigorously than in the pioneering work on the molecular epidemiology of tuberculosis (TB). Since the development of standardized methods for DNA fingerprinting of Mycobacterium tuberculosis, molecular techniques have been used to estimate the fraction of cases attributable to recent transmission of M. tuberculosis (7-14), identify host-specific risk factors for disease spread (15-18), document exogenous reinfection (19-21), and study patterns of drug resistance (22)(23)(24). Investigators also have begun to use these methods to explore potential strain-specific differences in bacterial phenotypes such as tissue tropism, virulence, and transmissibility (25,26).This research has shown that the genetic diversity of M. tuberculosis isolates from different human communities can vary considerably (27,28). Clusters of identical isolates are assumed to share DNA fingerprints as a result of the spread of the organism among the human hosts who harbor the isolates in the cluster. Patients with TB whose isolates cannot be grouped into clusters, i.e., those with unique DNA fingerprints, are assumed to have disease that results from the reactivation of latent infection acquired in the past. Variation in the distribution of clusters of M. tuberculosis isolates in different communities is thought to reflect different TB...

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“…No changes in fingerprint were found in a large number of sequential isolates from the same patients before and after acquired antibiotic resistance (Godfrey-Faussett et al 1993), suggesting the occurrence of mutations causing resistance instead of a selection of a resistant sub-population. Reinfection is the most probable mechanism underlying the fingerprint pattern change during development of drug resistance, as suggested by study of TB-patients in Hong Kong (Yuen et al 1995) and of HIV-infected patients (Small et al 1993b). In relation to the second question, many studies on fingerprinting of a large number of M. tuberculosis strains from specific populations looked for a correlation between strain clustering and drug resistance profile, so far without any evidence that a certain resistance is associated with a particular fingerprint type (e.g.…”

Section: Applications Of Molecular Strain Typing As An Additional Toomentioning

confidence: 99%

The Changing Face of the Epidemiology of Tuberculosis due to Molecular Strain Typing: A Review

Suffys¹,

Araujo²,

Degrave³

1997

Mem. Inst. Oswaldo Cruz

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Exogenous Reinfection with Multidrug-Resistant Mycobacterium tuberculosis in Patients with Advanced HIV Infection

Cited by 442 publications

References 21 publications

Antigen-Specific CD8+ T Cells and the Development of Central Memory during Mycobacterium tuberculosis Infection

Antigen-Specific CD8+ T Cells and the Development of Central Memory during Mycobacterium tuberculosis Infection

Determinants of cluster distribution in the molecular epidemiology of tuberculosis

The Changing Face of the Epidemiology of Tuberculosis due to Molecular Strain Typing: A Review

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