Experimental Treatment Greatly Decreases HIV Reactivation

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Compound reduces residual levels from infected dormant cells.

Compound reduces residual levels from infected dormant cells.

An experimental drug for HIV may hold the key to preventing reactivation of the virus after antiretroviral therapy is stopped.

Researchers from The Scripps Research Institute (TSRI) found that the natural compound Cortistatin A decreases residual viral levels from infected dormant cells. The compound established a near-permanent state of latency, which subsequently reduces the capacity of the virus to reactivate.

"Our results highlight an alternative approach to current anti-HIV strategies," said study lead Susana Valente in a press release. "Prior treatment with Cortistatin A significantly inhibits and delays viral rebound in the absence of any drug. Our results suggest current antiretroviral regimens could be supplemented with a Tat inhibitor, such as Cortistatin A, to achieve a functional HIV-1 cure, reducing levels of the virus and preventing reactivation from latent reservoirs."

In study published recently in the journal mBio, researchers evaluated the compound, which was originally isolated from a marine sponge, Corticium simplex, in 2006. TSRI investigators were able to synthesize the compound in 2008.

A configuration of the compound called didehydro-Cortistatin A was previously found to target the protein Tat, which significantly increases viral production. In the current study, didehydro-Cortistatin A was found to limit replication in HIV-infected cells by reducing viral messenger RNA levels.

"In latently infected primary T cells isolated from nine HIV-infected subjects being treated with antiretroviral drugs, didehydro-Cortistatin A reduced viral reactivation by an average of 92.3%," said first author Guillaume Mousseau.

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