Published in Blood Weekly, January 27th, 2005
"Substitution of the SIVmac239 promoter/enhancer by the strong EF1alpha promoter results in a severe replication defect due to a failure to respond to Tat. Revertant viruses with minimal promoter sequences (two Sp1 sites and a TATA box) were obtained that had fully restored their replicative 2 potential.
"Comparison of the different LTRs indicated that structural alterations in the TAR stem due to a 31 bp exon of the EF1alpha promoter rather than the mere presence of transcription factor binding sites within U3 were responsible for the attenuation," investigators in France...
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