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Cancer drug flushes dormant HIV out of hiding in the body

The compound reactivates latent virus cells so they can be killed by the immune system.

By Stephen Feller

SACRAMENTO, July 31 (UPI) -- The active ingredient in a cancer drug was found by researchers to reactivate latent human immunodefiency virus, or HIV, hiding in the body so that it can be killed by the immune system and anti-retroviral drugs.

Highly active anti-retroviral therapy, or HAART, is a three-drug combination that significantly reduces the level of virus in patients' systems. Once the treatment is discontinued, however, pools of latent virus reactivate and begin attacking the body again -- meaning patients risk long-term toxicity because they have to take the drugs indefinitely.

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"We are excited to have identified an outstanding candidate for HIV reactivation and eradication that is already approved and is being used in patients," said Satya Dandekar, chair of the Department of Medical Microbiology and Immunology at the University of California Davis, in a press release. "This molecule has great potential to advance into translational and clinical studies."

In looking for a drug that could reactivate latent virus cells, researchers said they needed to find proteins that would target HIV latency without overtaxing the immune system or activating other protein master switches, which can generate severe side effects.

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Researchers found that the active ingredient in the cancer drug PICATO, called PEP005, reactivated HIV cells in patient blood samples. When another compound called JQ1 was identified as working synergistically with PEP005, researchers saw HIV activation increase by about 15 times.

PICATO is already FDA-approved and in use with patients, in addition to the research showing it is less cytotoxic and doesn't cause major immune responses, Dandekar said. The work, however, is not done.

"We need to identify the best combination of latency-activating agents," said Dandekar. "Then we must help patients clear these reactivated cells. Just reactivating the HIV from latency won't be enough."

The study is published in PLOS Pathogens.

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