Affiliations: Institut Clínic de Infeccions i Immunitat, Barcelona, Spain,
Columbia University, New York, NY
Correspondence to: Àlex Soriano, MD, Servei de Malalties Infeccioses, Hospital Clínic Universitari, C/Villarroel 70, 08036 Barcelona, Spain; e-mail ASORIANO@clinic.ub.es
In a recent issue of CHEST, Schluger et al1–
(August 2002) reported on a very interesting study of the immune response against tuberculosis in HIV-infected patients who were receiving antiretroviral therapy. This finding is crucial in order to predict the relapse of tuberculosis infection and to develop new therapeutic approaches for HIV-infected people.2
However, there are some points in the study on which we would like to comment. (1) The proliferative response and amount of interferon-γ secretion when peripheral-blood mononuclear cells were stimulated with H37Ra were not different, based on previous tuberculin skin test results. In this respect, it is possible that live and heat-killed Mycobacterium tuberculosis H37Ra might not be specific. Thus, the results concerning immune reconstitution after antiretroviral therapy cannot be attributed to the restoration of the immune response against M tuberculosis. In order to clarify this question, it would also be interesting to know the results obtained when peripheral-blood mononuclear cells were stimulated with the other tested antigens (Mycobacterium bovis bacillus Calmette-Guerin-expressing strain and purified protein derivative). (2) The authors considered that all HIV-positive subjects were latently infected by M tuberculosis, because they were born outside the United States or they had risk factors for tuberculosis infection. However, the authors were not able to affirm the definitive diagnosis of latent M tuberculosis infection.
Taking into consideration all these facts, we believe that the conclusions of Schluger et al1
should be considered cautiously since there is no evidence that the antigen used was a specific one. In the future, it would probably be useful to perform a new study using more specific antigens3
and to include patients with documented active and latent M tuberculosis infection.
We agree with Dr. Soriano that the T-cell responses we described in our article may not be specific for Mycobacterium tuberculosis. However, we made no claim in the article that in fact they were specific. The article points out that there is a certain time course that describes the reconstitution of immune recognition of tuberculosis, and it is certainly reasonable to think, as Dr. Soriano suggests, that this description might apply to immune recognition of other pathogens as well.
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