DDX5 facilitates HIV-1 replication as a cellular co-factor of Rev

PLoS One. 2013 May 31;8(5):e65040. doi: 10.1371/journal.pone.0065040. Print 2013.

Abstract

HIV-1 Rev plays an important role in the late phase of HIV-1 replication, which facilitates export of unspliced viral mRNAs from the nucleus to cytoplasm in infected cells. Recent studies have shown that DDX1 and DDX3 are co-factors of Rev for the export of HIV-1 transcripts. In this report, we have demonstrated that DDX5 (p68), which is a multifunctional DEAD-box RNA helicase, functions as a new cellular co-factor of HIV-1 Rev. We found that DDX5 affects Rev function through the Rev-RRE axis and subsequently enhances HIV-1 replication. Confocal microscopy and co-immunoprecipitation analysis indicated that DDX5 binds to Rev and this interaction is largely dependent on RNA. If the DEAD-box motif of DDX5 is mutated, DDX5 loses almost all of its ability to bind to Rev, indicating that the DEAD-box motif of DDX5 is required for the interaction between DDX5 and Rev. Our data indicate that interference of DDX5-Rev interaction could reduce HIV-1 replication and potentially provide a new molecular target for anti-HIV-1 therapeutics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Active Transport, Cell Nucleus
  • Cell Line
  • DEAD-box RNA Helicases / genetics
  • DEAD-box RNA Helicases / metabolism*
  • Gene Expression
  • Genes, Reporter
  • HIV-1 / physiology*
  • Humans
  • Protein Binding
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Response Elements
  • Virus Replication*
  • rev Gene Products, Human Immunodeficiency Virus / metabolism*

Substances

  • RNA, Messenger
  • rev Gene Products, Human Immunodeficiency Virus
  • Ddx5 protein, human
  • DEAD-box RNA Helicases