Therapeutic Failure or Success Risk Associated with the Dynamic of Immunological Parameters in People Living with HIV-1 on Antiretroviral Treatment in Benin.

Until now, human immunodeficiency virus type 1 infection monitoring is based on plasma viral load and cluster of differentiation (CD)4-positive cells from thymus (CD4+ T cells) count. However, it is increasingly accepted that this biological monitoring should be strengthened with other markers that would reinforce the management. Therefore, we addressed this task by assessing the risk associated with therapeutic failure/success linked to the dynamic of immunological parameters in people living with HIV-1 (PLHIV-1) and on antiretroviral therapy (ART) in order to identify their prognostic values. Ninety enrolled PLHIV-1 were classified according to their therapeutic status. Twenty healthy persons were also recruited as a control group. Serum cytokine levels and immune cell frequencies were determined, and the risk of therapeutic failure associated with immunological parameters was assessed. We observed low frequencies of CD4+ T, natural killer (NK), natural killer T (NKT) cells, classical monocytes, nonclassical monocytes, granulocytes, and high frequency of CD8+ T cells in all PLHIV-1 groups in treatment failure under dolutegravir (DTG) and efavirenz (EFV) regimens compared to control participants. Moreover, interferon-gamma (IFN-γ) levels decreased in PLHIV-1 with therapeutic success under the DTG regimen, while interleukin-4 (IL-4) increased in treatment success under the EFV regimen. Proinflammatory tumor necrosis factor-alpha (TNF-α), IL-6, and IL-7 significantly increased in therapeutic failure groups under both regimens. IL-5 concentrations increased in all PLHIV-1, while IL-13 levels did not change. Logistic regression analysis revealed a positive correlation between the risk of treatment failure and proinflammatory cytokines IFN-γ, TNF-α, IL-6, IL-7, eosinophils, and CD8+ T cells in PLHIV-1 under EFV and DTG regimes. In contrast, the risk of therapeutic failure decreased with increasing numbers of CD4+ T cells, neutrophils, and the anti-inflammatory IL-4 in PLHIV-1 treated with the same antiretroviral molecules. Collectively, these results indicated that pro- and anti-inflammatory cytokines and immune cells could serve as prognostic factors for monitoring HIV-1 disease progression and response to ART. However, further studies with a larger sample size would be needed to confirm our data.