The human immunodeficiency virus (HIV) is a complicated one. Once it gets into the system, it can find its way into the DNA of the human cells where it can lay dormant for a period of years before it becomes active and develops into acquired immunodeficiency syndrome (AIDS). But a team has found a way to force the virus to awaken, so it's much easier to kill.
The cunning method in which the virus works has been a huge problem for researchers who are trying to curb the disease that affects 36.9 million people around the globe and causes the death of more than a million, according to World Health Organization (WHO) statistics.
So far, the only standard treatment is the antiretroviral drugs whose job is to prevent these viruses from replicating. They don't remove the virus out of the body.
The areas where these viruses are found are called reservoirs. The viruses, on the other hand, are known to have histone deactylase (HDAC), which wraps itself around the virus to keep it undetected. Thus, scientists are working on ways to produce the most potent HDAC inhibitor, and they may have found it in a cancer drug known as romidepsin, which is used for treating T-cell lymphoma.
The team recruited 6 Caucasians whose average age was 56. They had been on antiretroviral drugs for the past 10 years. For the study, each of the participants received a single romidepsin infusion every week within three weeks. Then their overall health, including adverse side effects, were followed up and monitored.
Although there were side effects, they were only minor. Most of all, all but one responded positively to the drug-that is, the drug was able to coax out the virus from the reservoirs without suppressing the body's immune system.
Despite the positive and promising results, the team believes it may still take at least a decade before a cure can be developed. The study is also small, but it can be a good precedent for future studies or basis for a follow-up, including combining the drug with HIV vaccine, which is the team's second stage for its clinical trial.
The study has been published in PLOS Pathogens since Sept 17.
