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10.1186/s12977-015-0174-4

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suck abstract from ncbi


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pmid26032178
      Retrovirology 2015 ; 12 (ä): 46
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  • SAMHD1 specifically restricts retroviruses through its RNase activity #MMPMID26032178
  • Choi J ; Ryoo J ; Oh C ; Hwang S ; Ahn K
  • Retrovirology 2015[Jun]; 12 (ä): 46 PMID26032178 show ga
  • BACKGROUND: Human SAMHD1 possesses dual enzymatic functions. It acts as both a dGTP-dependent triphosphohydrolase and as an exoribonuclease. The dNTPase function depletes the cellular dNTP pool, which is required for retroviral reverse transcription in differentiated myeloid cells and resting CD4(+) T cells; thus this activity mainly plays a role in SAMHD1-mediated retroviral restriction. However, a recent study demonstrated that SAMHD1 directly targets HIV-1 genomic RNA via its RNase activity, and that this function (rather than dNTPase activity) is sufficient for HIV-1 restriction. While HIV-1 genomic RNA is a potent target for SAMHD1 during viral infection, the specificity of SAMHD1-mediated RNase activity during infection by other viruses is unclear. RESULTS: The results of the present study showed that SAMHD1 specifically degrades retroviral genomic RNA in monocyte-derived macrophage-like cells and in primary monocyte-derived macrophages. Consistent with this, SAMHD1 selectively restricted retroviral replication, but did not affect the replication of other common non-retro RNA genome viruses, suggesting that the RNase-mediated antiviral function of SAMHD1 is limited to retroviruses. In addition, neither inhibiting reverse transcription by treatment with several reverse transcriptase inhibitors nor infection with reverse transcriptase-defective HIV-1 altered RNA levels after viral challenge, indicating that the retrovirus-specific RNase function is not dependent on processes associated with retroviral reverse transcription. CONCLUSIONS: The results presented herein suggest that the RNase activity of SAMHD1 is sufficient to control the replication of retroviruses, but not that of non-retro RNA viruses.
  • |*Host-Pathogen Interactions [MESH]
  • |*Immunity, Innate [MESH]
  • |*Virus Replication [MESH]
  • |Cell Line [MESH]
  • |Humans [MESH]
  • |Hydrolysis [MESH]
  • |Macrophages/immunology/virology [MESH]
  • |Monomeric GTP-Binding Proteins/*metabolism [MESH]
  • |RNA, Viral/*metabolism [MESH]
  • |Retroviridae/*immunology/physiology [MESH]
  • |Ribonucleases/*metabolism [MESH]


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