HIV-1 replication in human immune cells is independent of TAR DNA binding protein 43 (TDP-43) expression

PLoS One. 2014 Aug 15;9(8):e105478. doi: 10.1371/journal.pone.0105478. eCollection 2014.

Abstract

The TAR DNA binding protein (TDP-43) was originally identified as a host cell factor binding to the HIV-1 LTR and thereby suppressing HIV-1 transcription and gene expression (Ou et al., J.Virol. 1995, 69(6):3584). TDP-43 is a global regulator of transcription, can influence RNA metabolism in many different ways and is ubiquitously expressed. Thus, TDP-43 could be a major factor restricting HIV-1 replication at the level of LTR transcription and gene expression. These facts prompted us to revisit the role of TDP-43 for HIV-1 replication. We utilized established HIV-1 cell culture systems as well as primary cell models and performed a comprehensive analysis of TDP-43 function and investigated its putative impact on HIV-1 gene expression. In HIV-1 infected cells TDP-43 was neither degraded nor sequestered from the nucleus. Furthermore, TDP-43 overexpression as well as siRNA mediated knockdown did not affect HIV-1 gene expression and virus production in T cells and macrophages. In summary, our experiments argue against a restricting role of TDP-43 during HIV-1 replication in immune cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Gene Expression
  • Gene Expression Regulation, Viral
  • Genes, Viral
  • HEK293 Cells
  • HIV Long Terminal Repeat
  • HIV-1 / physiology*
  • Humans
  • Jurkat Cells
  • Protein Transport
  • Transcriptional Activation
  • Virus Replication*

Substances

  • DNA-Binding Proteins
  • TARDBP protein, human

Grants and funding

Financial support for this study was provided by intramural funding of the Helmholtz Zentrum München. JN and MS received funding from the German Research Foundation (DFG SCHI1073/4-1) and the Else Kröner-Fresenius Stiftung. TF was supported by the KNDD2 grants FKZ 01 GI 1005D. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.