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SAMHD1 restricts HIV-1 reverse transcription in quiescent CD4+T-cells
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SAMHD1 restricts HIV-1 reverse transcription in quiescent CD4+T-cells
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SAMHD1 restricts HIV-1 reverse transcription in quiescent CD4+T-cells
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Journal Article
SAMHD1 restricts HIV-1 reverse transcription in quiescent CD4+T-cells
2012
Overview
Background
Quiescent CD4
+
T lymphocytes are highly refractory to HIV-1 infection due to a block at reverse transcription.
Results
Examination of SAMHD1 expression in peripheral blood lymphocytes shows that SAMHD1 is expressed in both CD4+ and CD8+ T cells at levels comparable to those found in myeloid cells. Treatment of CD4+ T cells with Virus-Like Particles (VLP) containing Vpx results in the loss of SAMHD1 expression that correlates with an increased permissiveness to HIV-1 infection and accumulation of reverse transcribed viral DNA without promoting transcription from the viral LTR. Importantly, CD4
+
T-cells from patients with Aicardi-Goutières Syndrome harboring mutation in the
SAMHD1
gene display an increased susceptibility to HIV-1 infection that is not further enhanced by VLP-Vpx-treatment.
Conclusion
Here, we identified SAMHD1 as the restriction factor preventing efficient viral DNA synthesis in non-cycling resting CD4
+
T-cells. These results highlight the crucial role of SAMHD1 in mediating restriction of HIV-1 infection in quiescent CD4
+
T-cells and could impact our understanding of HIV-1 mediated CD4
+
T-cell depletion and establishment of the viral reservoir, two of the HIV/AIDS hallmarks.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Biomedical and Life Sciences
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - virology
/ DNA
/ Genes
/ HIV
/ HIV-1
/ Human immunodeficiency virus
/ Humans
/ Monomeric GTP-Binding Proteins - immunology
/ Monomeric GTP-Binding Proteins - metabolism
/ SAM Domain and HD Domain-Containing Protein 1
/ SAMHD1
/ T cells
/ Vaccine
/ Viral Regulatory and Accessory Proteins - immunology
/ Viral Regulatory and Accessory Proteins - metabolism
/ Virology
