Over-expression of the HIV-1 Rev promotes death of nondividing eukaryotic cells

Aviad Levin, Zvi Hayouka, Assaf Friedler, Abraham Loyter*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Expression of the human immunodeficiency virus type 1 (HIV-1) Rev protein is essential for completion of the viral life cycle. Rev mediates nuclear export of partially spliced and unspliced viral transcripts and therefore bears a nuclear localization signal (NLS) as well as a nuclear export signal (NES), which allow its nucleocytoplasmic shuttling. Attempts to express the wild-type Rev protein in eukaryotic human cultured cells have encountered difficulties and so far have failed. Here we show that accumulation of Rev, which occurs in nondividing Revexpressing cells or when such cells reach confluency, results in death of these cells. Cell death was also promoted by addition of a cell permeable peptide bearing the Rev-NES sequence, but not by the Rev-NLS peptide. Our results probably indicate that binding of excess amounts of the Rev protein or the NES peptide to the exportin receptor CRM1 results in cells' death.

Original languageAmerican English
Pages (from-to)341-346
Number of pages6
JournalVirus Genes
Issue number3
StatePublished - Jun 2010

Bibliographical note

Funding Information:
Acknowledgments This study was supported by the Israeli Science Foundation (AL) and by a starting grant from the European Research Council (ERC) (to AF).


  • Cell death
  • HIV-1
  • Nucleocytoplasmic shuttling
  • Rev
  • Stable expression


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