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SAMHD1 does it again, now in resting T cells

Nature Medicine volume 18, pages1611–1612(2012)Cite this article

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A long-standing question in the HIV field is why HIV-1 fails to replicate in resting CD4+ T cells. A new study shows that host deoxynucleoside triphosphate triphosphohydrolase (dNTPase) sterile α motif and histidine/aspartic domain–containing protein 1 (SAMHD1), previously shown to block HIV infection in myeloid cells, also restricts HIV replication in resting CD4+ T cells by hydrolyzing dNTPs, which are needed for reverse transcription of the virus (pages 1682–1687).

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Figure 1: SAMHD1 restricts HIV-1 replication in resting CD4+ T cells by reducing dNTP concentrations needed for reverse transcription.

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Affiliations

  1. Nan Yan is in the Department of Internal Medicine and Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.

    Nan Yan

  2. and Department of Pediatrics, Judy Lieberman is in the Program in Cellular and Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

    Judy Lieberman

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  1. Nan Yan
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  2. Judy Lieberman
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Correspondence to Nan Yan or Judy Lieberman.

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The authors declare no competing financial interests.

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Yan, N., Lieberman, J. SAMHD1 does it again, now in resting T cells. Nat Med 18, 1611–1612 (2012). https://doi.org/10.1038/nm.2980

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