Abstract

Background Tat, the HIV Trans-Activator of Transcription is a potential antiviral target. Tat binds to the 5’ terminal region of HIV mRNAs stem-bulge-loop structure called the Trans-activation Responsive (TAR) element and activates transcription from the HIV promoter. Plasma viremia stubbornly persists in HIV-1 infected subjects despite receiving HAART, suggesting that residual levels of viral production originate from an integrated form of the HIV genome that is continuously transcribed at low levels. As current antiretrovirals (ARVs) fail to inhibit transcription from integrated viral genomes or viral production from stable cellular reservoirs, novel classes of ARVs are needed to inhibit this process.

Highlights

  • Tat, the HIV Trans-Activator of Transcription is a potential antiviral target

  • Plasma viremia stubbornly persists in HIV-1 infected subjects despite receiving HAART, suggesting that residual levels of viral production originate from an integrated form of the HIV genome that is continuously transcribed at low levels

  • Cortistatin A is a steroidal alkaloid isolated from the marine sponge Corticium simplex

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Summary

Open Access

Guillaume Mousseau, Mark A Clementz, Wendy N Bakeman, Nisha Nagarsheth, Michael Cameron, Jun Shi, Phil Baran, Rémi Fromentin, Nicolas Chomont, Susana T Valente1*. From 17th International Symposium on HIV and Emerging Infectious Diseases (ISHEID) Marseille, France. 23-25 May 2012

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