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CD4+ T-cell differentiation, regulatory T cells and gag-specific T lymphocytes are unaffected by CD4-guided treatment interruption and therapy resumption

Objectives:Despite limiting exposure to antiretroviral drugs, structured treatment interruptions can influence multiple aspects of T-cell immunity, particularly those regarding CD4+ T lymphocytes. We evaluated the impact of CD4-guided treatment interruption (CD4-GTI) and treatment resumption on regulatory T cells (Tregs), T-lymphocyte activation, differentiation and polyfunctional gag-specific response. Methods:Patients were analyzed just prior to treatment interruption, at 2 and 6 months after treatment interruption, just prior to treatment resumption and at 2 and 6 months after treatment resumption. Thawed peripheral blood mononuclear cells were stained immediately for phenotype analysis or stimulated with HIV-gag peptides and analyzed by polychromatic flow cytometry. Results:Treatment interruption resulted in a CD4+ cell count decrease and plasma viral load (pVL) increase, but did not preclude a good immune reconstitution and a complete suppression of pVL after treatment resumption. Treatment interruption did not influence CD4+ T-cell differentiation and Treg subsets. During treatment interruption, gag-specific CD4+ T cells were not lost, although the frequency of HIV-specific CD8+ cells increased. Most gag-specific CD4+ T cells were potentially cytotoxic (CD107a+) and were not influenced by pVL or by HAART. Most helper (CD154+) gag-specific CD4+ T lymphocytes did not produce interferon-&ggr; or interleukin-2. Conclusion:CD4-GTI did not cause depletion of memory cells, Tregs or HIV-specific CD4+ cells and, on the contrary, could induce HIV-specific responses. If guided by CD4+ T-cell count, treatment interruption does not provoke irreversible immune damages.