SAMHD1 restricts HIV-1 reverse transcription in quiescent CD4+ T-cells

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• 作者：Benjamin Descours (1)
  Alexandra Cribier (1)
  Christine Chable-Bessia (1)
  Diana Ayinde (3)
  Gillian Rice (2)
  Yanick Crow (2)
  Ahmad Yatim (1)
  Olivier Schwartz (3)
  Nadine Laguette (1)
  Monsef Benkirane (1)
  
• 关键词：SAMHD1 ; Quiescent CD4+ T ; cell ; HIV ; 1 ; Reverse transcription ; Restriction
• 刊名：Retrovirology
• 出版年：2012
• 出版时间：December 2012
• 年：2012
• 卷：9
• 期：1
• 全文大小：410KB
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• 作者单位：Benjamin Descours (1)
  Alexandra Cribier (1)
  Christine Chable-Bessia (1)
  Diana Ayinde (3)
  Gillian Rice (2)
  Yanick Crow (2)
  Ahmad Yatim (1)
  Olivier Schwartz (3)
  Nadine Laguette (1)
  Monsef Benkirane (1)
  
  1. Institut de Génétique Humaine, CNRS UPR1142, Laboratoires de Virologie Moléculaire, Montpellier, France
  3. Institut Pasteur, Virus and Immunity Unit, URA CNRS, 3015, Paris, France
  2. Academic Unit of Medical Genetic, University of Manchester, Manchester, UK
  
• ISSN：1742-4690

文摘

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.