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Reconstitution of Immune Responses to Tuberculosis in Patients With HIV Infection Who Receive Antiretroviral Therapy^*

^* From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY.

Correspondence to: Neil W. Schluger, MD, FCCP, Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, PH-8 Center, 630 West 168th St, New York, NY 10032; e-mail: ns311{at}columbia.edu

Study objectives: To assess the restoration of immune responses to tuberculosis, as manifested by secretion of T-helper type 1 cytokines (interferon [IFN]-, interleukin [IL]-12, and IL-2) and T-helper type 2 cytokines (IL-10), in HIV-positive patients who receive antiretroviral therapy (ART).

Design: Prospective cohort study.

Setting: University hospital.

Patients: Ten HIV-positive patients, all naïve to ART and all about to start ART for clinical indications, and 11 healthy, HIV-negative control subjects.

Interventions: Assessment of T-cell proliferation and cytokine production after administration of ART to patients with HIV infection.

Measurements and results: All patients had a negative tuberculin skin test result at baseline and were anergic. Highly active ART reduced the viral load to very low levels in all patients within a short time after starting therapy. Blood samples were drawn every 2 months after starting therapy, and continued for 1 year while the patients continued to receive ART. There were trends toward increased proliferation of peripheral blood mononuclear cells (PBMCs) in response to Mycobacterium tuberculosis-specific stimuli, but these were delayed until several months of ART had elapsed. Similar trends were noted in relation to the secretion of IFN-. Neither PBMC proliferation nor IFN- secretion reached levels seen in healthy control subjects. No consistent trends in IL-2, IL-10, or IL-12 production were noted.

Conclusion: ART restores immune responses to M tuberculosis, although this restoration is delayed and does not reach levels seen in healthy, HIV-negative control subjects. These results may explain in part the phenomenon of paradoxic reactions to antituberculosis therapy in patients with HIV infection. A larger study in which patients are followed up for a longer period of time will allow the magnitude and timing of this reconstitution to be more precisely defined.

Key Words: AIDS • immunity • treatment • tuberculosis

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