Abstract
CD4+ T cells are critical players in the host adaptive immune response. Emerging evidence suggests that certain CD4+ T cell subsets contribute significantly to the production of neutralizing antibodies and help in the control of virus replication. Circulating T follicular helper cells (Tfh) constitute a key T cell subset that triggers the adaptive immune response and stimulates the production of neutralizing antibodies (NAbs). T cells having stem cell-like property, called stem-like memory T cells (Tscm), constitute another important subset of T cells that play a critical role in slowing the rate of disease progression through the differentiation and expansion of different types of memory cell subsets. However, the role of these immune cell subsets in T cell homeostasis, CD4+ T cell proliferation, and progression of disease, particularly in HIV-2 infection, has not yet been elucidated. The present study involved a detailed evaluation of the different CD4+ T cell subsets in HIV-2 infected persons with a view to understanding the role of these immune cell subsets in the better control of virus replication and delayed disease progression that is characteristic of HIV-2 infection. We observed elevated levels of CD4+ Tfh and CD4+ Tscm cells along with memory and effector T cell abundance in HIV-2 infected individuals. We also found increased frequencies of CXCR5+ CD8+ T cells and CD8+ Tscm cells, as well as memory B cells that are responsible for NAb development in HIV-2 infected persons. Interestingly, we found that the frequency of memory CD4+ T cells as well as memory B cells correlated significantly with neutralizing antibody titers in HIV-2 infected persons. These observations point to a more robust CD4+ T cell response that supports B cell differentiation, antibody production, and CD8+ T cell development in HIV-2 infected persons and contributes to better control of the virus and slower rate of disease progression in these individuals.
Highlights
Acquired immunodeficiency in humans is caused by two types of human immunodeficiency virus (HIV), namely HIV-1 and HIV-2 [1]
Recent studies suggest that follicular CXCR5+ CD8+ T cells and CD8+ stem-like memory cells are involved in the control of HIV/ SIV infection [29, 30]
It may be assumed that elevated effector and memory cell differentiation could contribute to better control of viremia and slower disease progression in controllers of HIV infection [46]
Summary
Acquired immunodeficiency in humans is caused by two types of human immunodeficiency virus (HIV), namely HIV-1 and HIV-2 [1]. Unlike the case in HIV-1 infection, reduction in CD4+ T cells is much slower in HIV-2 infection [2]. Several studies have documented the significance of antiviral CD4+ as well as CD8+ T cells in the control of infection in HIV-1 non-progressors and HIV-2 slow progressors [3,4,5,6,7]. Studies have shown differences in levels of expression of immune activation as well exhaustion markers including HLADR, PD1, CCR5, SAMHD1, Blimp-1 and TRIM5a on CD4+ T cell subsets in HIV-1 and HIV-2 infected individuals [8]. Other factors that have been implicated in slower disease progression associated with HIV-2 infection include higher frequencies of virus-specific highly differentiated polyfunctional T cells and high titers of neutralizing antibodies [7, 9]. The role of recently identified CD4+ T cell subsets like the T follicular helper cells and stem cell like memory T cells that are known to play a critical role in the control of HIV infection have not been investigated in the context of HIV-2 infection
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