Abstract
Treatment of persons with latent tuberculosis (TB) infection at greatest risk of reactivation is an important component of TB control and elimination strategies. Biomarkers evaluating the effectiveness of treatment of latent TB infection have not yet been identified. This information would enhance control efforts and assist the evaluation of new treatment regimes.
We designed a two-group, two-arm, randomised clinical study of tuberculin skin test-positive participants: 26 with documented contact with TB patients and 34 with non-documented contact. Participants in each group were randomly assigned to the immediate- or deferred-isoniazid treatment arms. Assays of in vitro interferon (IFN)-γ secretion in response to recombinant Rv1737 and overlapping synthetic peptide pools from various groups of immunodominant proteins were performed.
During isoniazid therapy, a significant increase from baseline in the proportion of IFN-γ responders to the 10-kDa culture filtrate protein, Rv2031, Rv0849, Rv1986, Rv2659c, Rv2693c and the recombinant Rv1737 protein was observed (p⩽0.05). The peptide pool of Rv0849 and Rv1737 recombinant proteins induced the highest percentage of IFN-γ responders after isoniazid therapy.
The in vitro IFN-γ responses to these proteins might represent useful markers to evaluate changes associated with treatment of latent TB infection.
Abstract
Peptide pool of Rv0849 and recombinant protein Rv1737 may be useful to test the efficacy of treatment of latent TB http://ow.ly/Catld
Footnotes
This article has supplementary material available from erj.ersjournals.com
Clinical trial: This study was registered at www.ClinicalTrials.gov with identifier number NCT00293228
Support statement: This work was funded by the Bill and Melinda Gates Foundation (grants GCGH#11 reference 37222 and GCGH #6-74), the US National Institutes of Health (A135969 and K01TW000001), the Wellcome Trust (176W009, 084323 and 088316), the Howard Hughes Medical Institute (55000632) and CONACYT (SALUD 2003-C01-132, SEP-2004-C01-47499/A1, FOSSIS 2005-03 (15203), FOSSIS 2005-2 (14475), SALUD-2008-C01-87332 and SALUD-2010-01-140178). R.J. Wilkinson also received support from the UK Medical Research Council (U1175.02.002.00014.01) and the European Union.
Conflict of interest: Disclosures can be found alongside the online version of this article at erj.ersjournals.com
- Received July 4, 2014.
- Accepted September 16, 2014.
- Copyright ©ERS 2015
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