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Human Immunodeficiency Virus (HIV) has the capability to enter a latent stage of infection where it exists as a dormant provirus in CD4+ T-cells.Most latently infected cells are resting memory T cells, [1] however a small fraction of latently infected cells isolated from HIV patients are naive CD4 T cells.
Studies suggest that only ~5% of the lymphoid-derived CD4 T cells targeted by HIV are permissive and become productively infected with the virus. More than 95% of the CD4 T cells that die are resting and are unable to support productive infection. These cells undergo abortive infection with HIV. [36]
In immunology, a naive T cell (T h 0 cell) is a T cell that has differentiated in the thymus, and successfully undergone the positive and negative processes of central selection in the thymus. Among these are the naive forms of helper T cells ( CD4 + ) and cytotoxic T cells ( CD8 + ).
The reason for the preferential loss of mucosal CD4 + T cells is that a majority of mucosal CD4 + T cells express the CCR5 coreceptor, whereas a small fraction of CD4 + T cells in the bloodstream do so. [5] HIV seeks out and destroys CCR5 expressing CD4 + cells during acute infection. A vigorous immune response eventually controls the infection ...
HIV-1 uses CD4 to gain entry into host T-cells and achieves this through its viral envelope protein known as gp120. [19] The binding to CD4 creates a shift in the conformation of gp120 allowing HIV-1 to bind to a co-receptor expressed on the host cell. These co-receptors are chemokine receptors CCR5 or CXCR4.
Optimal CD8 + T cell response relies on CD4 + signalling. [44] CD4 + cells are useful in the initial antigenic activation of naive CD8 T cells, and sustaining memory CD8 + T cells in the aftermath of an acute infection. Therefore, activation of CD4 + T cells can be beneficial to the action of CD8 + T cells. [45] [46] [47]
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