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Impact of viral accessory proteins of SIVsmmPBj on early steps of infection of quiescent cells.

Abstract
Although lentiviruses like HIV-1 are able to infect non-dividing cells, particular resting cells such as non-stimulated primary peripheral blood mononuclear cells (PBMC) are resistant to infection. In contrast to other lentiviruses, SIVsmmPBj can replicate in non-stimulated PBMC. Moreover, SIVsmmPBj-derived, but not HIV-1-derived, replication-incompetent vectors enable gene transfer into G(0)-arrested human cell lines and primary human monocytes. Here, we demonstrate that transduction of G(0)-arrested cell lines by SIVsmmPBj-derived vectors is independent of the viral accessory proteins Vif, Vpx, Vpr, or Nef. In contrast, for the transduction of primary human monocytes, the Vpx protein proved to be essential. However, trans-complementation of HIV-1 vectors with SIVsmmPBj Vpx did not provide the property of gene transfer into monocytes. Taken together, these data indicate that Vpx is essential for the infection of primary monocytes by SIVsmmPBj. Additionally, further genome functions besides the accessory proteins are required for the particular capacity of SIVsmmPBj in transduction or infection events.
AuthorsNina Wolfrum, Michael D Mühlebach, Silke Schüle, Julia K Kaiser, Björn-Philipp Kloke, Klaus Cichutek, Matthias Schweizer
JournalVirology (Virology) Vol. 364 Issue 2 Pg. 330-41 (Aug 1 2007) ISSN: 0042-6822 [Print] United States
PMID17418360 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • DNA, Viral
  • Retroviridae Proteins
  • VPX protein, Simian immunodeficiency virus
  • Viral Regulatory and Accessory Proteins
Topics
  • Base Sequence
  • Cell Line
  • DNA, Viral (genetics)
  • G0 Phase
  • Gene Deletion
  • Genes, Viral
  • Genetic Complementation Test
  • Genetic Vectors
  • HIV (genetics)
  • Humans
  • Monocytes (virology)
  • Retroviridae Proteins (genetics, physiology)
  • Simian Immunodeficiency Virus (genetics, pathogenicity, physiology)
  • Transduction, Genetic
  • Viral Regulatory and Accessory Proteins (genetics, physiology)
  • Virus Replication

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