A drug used to treat chronic alcoholism shows potent ability to wake up dormant Human Immunodeficiency Virus hiding in cells, making them an easy target to be killed. The finding may pave way for the development of HIV cure.

Published in the journal, The Lancet HIV, researchers from the University of Melbourne and the University of California, San Francisco found that disulfiram (trade name Antabuse), a commonly-used drug for alcoholism that produces hangover-like symptoms when alcohol is consumed, could activate 'sleeping' HIV hiding in the cells of the body.

HIV is a growing epidemic worldwide. Around 35 million people are living with HIV and 2.1 million new cases were diagnosed in 2013, according to the Centers for Disease Control and Prevention. In the United States alone, 47,500 new HIV infections were recorded in 2010.

The virus is considered a 'smart' pathogen because of its ability to integrate itself into the DNA of its host's cells. This creates a masking effect on the virus as it goes into latency that can last for years, hiding from the body's immune system.

Anti-retroviral therapy (ART) is the main treatment used to kill HIV in the body. Though people who are taking the medicine experience a reduction in the number of the virus, not all are killed. These viruses that lay dormant and hiding inside cells could potentially proliferate in the future.

The researchers tested the drug on 30 patients who were also taking ART. For three days, the patients were given increasing doses of disulfiram (500 mg, 1,000 mg and 2,000 mg). The first two doses did not lead to significant effects, but after the patients received the 2,000 mg dose of the drug, it re-activated dormant HIV in the body.

Seven days after the last dose of drug was given, the number of virus RNA found in the blood increased by as much as 75 percent. Around 30 days after the treatment, the number increased to 100 percent.

Waking up the virus was just the first step of the process. "The next step is to get these cells to die," said Julian Elliott of the department of infectious diseases at the Alfred hospital in Melbourne.

"The dosage of disulfiram we used provided more of a tickle than a kick to the virus, but this could be enough. Even though the drug was only given for three days, we saw a clear increase in [the] virus in [blood] plasma, which was very encouraging," explained Sharon Lewin, who is a professor at the University in Melbourne and one of the authors of the study.

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