Abstract
The combination antiretroviral therapeutic (cART) regime effectively suppresses human immunodeficiency virus (HIV) replication and prevents progression to acquired immunodeficiency diseases. However, cART is not a cure, and viral rebound will occur immediately after treatment is interrupted largely due to the long-term presence of an HIV reservoir that is composed of latently infected target cells that maintain a quiescent state or persistently produce infectious viruses. CD4 T cells that reside in B-cell follicles within lymphoid tissues, called follicular helper T cells (TFH), have been identified as a major HIV reservoir. Due to their specialized anatomical structure, HIV-specific CD8 T cells are largely insulated from this TFH reservoir. It is increasingly clear that the elimination of TFH reservoirs is a key step toward a functional cure for HIV infection. Recently, several studies have suggested that a fraction of HIV-specific CD8 T cells can differentiate into a CXCR5-expressing subset, which are able to migrate into B-cell follicles and inhibit viral replication. In this review, we discuss the differentiation and functions of this newly identified CD8 T-cell subset and propose potential strategies for purging TFH HIV reservoirs by utilizing this unique population.
Highlights
Human immunodeficiency virus (HIV)-specific CD8 T cells play an important role in suppressing human immunodeficiency virus (HIV) replication [1,2,3,4,5]
We focus on understanding the properties of HIV-specific CXCR5-expressing follicular cytotoxic cells and propose strategies for the functional cure of HIV infection by combining combination antiretroviral therapeutic (cART) and CXCR5+CD8 T cells
These similar characteristics of CXCR5+CD8 T cells during both chronic lymphocytic choromeningitis virus (LCMV) and HIV infection indicate that the differentiation of this unique subset might represent a common mechanism for defense against chronic viral infection
Summary
Human immunodeficiency virus (HIV)-specific CD8 T cells play an important role in suppressing HIV replication [1,2,3,4,5]. HIVspecific CXCR5+CD8 T cells exhibit a reduction in Id2 expression compared to HIV-specific CXCR5−CD8 T cells These similar characteristics of CXCR5+CD8 T cells during both chronic LCMV and HIV infection indicate that the differentiation of this unique subset might represent a common mechanism for defense against chronic viral infection. Intra-vital multi-photon confocal microscopy represents a reliable tool to visualize the dynamics of follicular-residing lymphocytes in a real-time pattern, which may provide more solid evidence as to the exact locations of virus-specific CXCR5+CD8 T cells in lymphoid tissues during chronic viral infection Both studies found that CXCR5+CD8 T cells preserved a better proliferative potential than CXCR5−CD8 T cells [45, 52]. In LCMV-Cl13 infection, compared to CXCR5−CD8 T cells, virusspecific CXCR5+CD8 T cells exhibit elevated effector cytokine
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