Journal
VIRUSES-BASEL
Volume 14, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/v14030581
Keywords
human immunodeficiency virus (HIV); simian immunodeficiency virus (SIV); immune checkpoint; immune checkpoint blocker; HIV therapy
Categories
Funding
- CAMS Innovation Fund for Medical Sciences [2021-I2M-1-037]
- National Natural Science Foundation of China [81971944]
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During HIV/SIV infection, upregulated immune checkpoint markers can lead to chronic T cell exhaustion and regulate disease progression by mediating T cell responses and enriching viral reservoirs. Overexpression of these markers inhibits cell proliferation and cytokine production, affecting viral persistence. Targeting immune checkpoints has shown potential therapeutic efficacy in HIV treatment.
During HIV/SIV infection, the upregulation of immune checkpoint (IC) markers, programmed cell death protein-1 (PD-1), cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4), T cell immunoglobulin and ITIM domain (TIGIT), lymphocyte-activation gene-3 (LAG-3), T cell immunoglobulin and mucin domain-3 (Tim-3), CD160, 2B4 (CD244), and V-domain Ig suppressor of T cell activation (VISTA), can lead to chronic T cell exhaustion. These ICs play predominant roles in regulating the progression of HIV/SIV infection by mediating T cell responses as well as enriching latent viral reservoirs. It has been demonstrated that enhanced expression of ICs on CD4(+) and CD8(+) T cells could inhibit cell proliferation and cytokine production. Overexpression of ICs on CD4(+) T cells could also format and prolong HIV/SIV persistence. IC blockers have shown promising clinical results in HIV therapy, implying that targeting ICs may optimize antiretroviral therapy in the context of HIV suppression. Here, we systematically review the expression profile, biological regulation, and therapeutic efficacy of targeted immune checkpoints in HIV/SIV infection.
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