Commentary
Inhibition of HIV-1 gene expression by Sam68ΔC: multiple targets but a common mechanism?
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Correspondence: Alan Cochrane alan.cochrane@utoronto.ca
Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada
Retrovirology 2009, 6:22 doi:10.1186/1742-4690-6-22
Published: 2 March 2009Abstract
Two recent publications have explored the mechanisms by which a mutant of the host protein Sam68 blocks HIV-1 structural protein synthesis and expands its activity to encompass Nef. Although the two studies propose different mechanisms for the responses observed, it is possible that a common activity is responsible. Understanding how this Sam68 mutant discriminates among the multiple viral mRNAs promises to reveal unique properties of HIV-1 RNA metabolism.