The Synthetic CD4 Exocyclic CDR3.AME(82-89) Inhibits NF-kappaB Nuclear Translocation, HIV-1 Promoter Activation, and Viral Gene Expression

Roland, Joachim; Berezov, Alan; Greene, Mark I.; Murali, Ramachandran; Piatier-Tonneau, Dominique; Devaux, Christian; Briant, Laurence
November 1999
DNA & Cell Biology;Nov99, Vol. 18 Issue 11, p819
Academic Journal
We have previously shown that the synthetic aromatically modified exocyclic (AME) analog (CDR3.AME(82-89), derived from the CDR3 (residues 82-89) region of CD4 domain 1, inhibits replication of human immunodeficiency virus type 1 (HIV-1) in infected cells. In this work, we investigated the mechanism by which this inhibition is achieved. Although cells exposed to HIV-1 and treated with the CDR3.AME(82-89) peptide did not release viral particles for more than a week and kept surface expression of CD4, viral DNA was found in those cells 24 h after virus exposure, indicating that the CDR3.AME(82-89) analog does not prevent virus entry. However, virus transcription remained extremely low in infected cells, as demonstrated by the study of spliced HIV-1 mRNA in cultures treated with CDR3.AME(82-89) 72 h postinfection. Finally, the CDR3.AME(82-89) peptide was found to be a potent inhibitor of HIV-1 promoter activity and nuclear factor-kappaB translocation, indicating that the antiviral property of this peptide is, at least in part, linked with the ability of the molecule to prevent HIV-1 transcription.


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