Abstract
Since highly active antiretroviral treatment (HAART) regimens became widely available in North America and Europe in 1996, the incidence of AIDS-defining opportunistic infections and malignancies has declined dramatically. This decline has been attributed to restoration of protective immunity by HAART since HAART improves many of the deficits in T and B cell function that are caused by uncontrolled HIV infection. Some of these deficits include diminished antigen-specific T cell proliferation and cytokine expression, decreased production of new naive T cells by the thymus, and abnormally high levels of CD4+ and CD8+ T cell and B cell activation [1–3]. However, the causal link between the reversal or prevention of these T and B cell functional abnormalities and immune protection against AIDS-defining opportunistic infections and malignancies remains largely hypothetical at present.
Highlights
Since highly active antiretroviral treatment (HAART) regimens became widely available in North America and Europe in 1996, the incidence of AIDS-defining opportunistic infections and malignancies has declined dramatically
This means that potential correlates of protective immunity can be identified by comparing immunoassay results in patients who have clear evidence of absent CMVprotective immunity to those in patients who have clear evidence of restored CMV-protective immunity
We recently identified a pattern of immune function that was completely absent in the peripheral blood mononuclear cells (PBMC) of 100% of 24 patients with active CMV retinitis but was partially or completely present in the PBMC of 85% of 34 patients with CMV retinitis patients who had been clinically immuno-restored by HAART [4]
Summary
The best evidence for HAART-induced immune reconstitution translating into protective immunity is for AIDSrelated cytomegalovirus (CMV) retinitis. This means that potential correlates of protective immunity can be identified by comparing immunoassay results in patients who have clear evidence of absent CMVprotective immunity (i.e., patients with AIDS with active CMV retinitis) to those in patients who have clear evidence of restored CMV-protective immunity (i.e., patients with AIDS and CMV retinitis who, after HAART, are able to discontinue anti-CMV therapy without further retinitis reactivation or progression). We recently identified a pattern of immune function that was completely absent in the peripheral blood mononuclear cells (PBMC) of 100% of 24 patients with active CMV retinitis but was partially or completely present in the PBMC of 85% of 34 patients with CMV retinitis patients who had been clinically immuno-restored by HAART [4]. Larger, longitudinal, observational studies are needed to determine the predictive value and potential clinical utility of such immunoassays in defining CMVprotective immunity and guiding clinical management for patients with AIDS with a history of CMV retinitis or at risk for developing CMV retinitis
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