US-based scientists have developed an experimental drug compound that has shown promising results against the AIDS causing virus called Human Immunodeficiency Virus (HIV).
The novel drug candidate has been developed by the scientists at more than dozen of institutes, including the Scripps Research Institute in Florida and Harvard Medical School.
The scientists tested the experimental drug on monkeys (rhesus macaques) which can get infected from simian HIV, a virus that is similar to the HIV that infects humans.
During the clinical procedure, it was found that macaques inoculated with a compound called eCD4-lg, which is present in the drug, didn’t catch the simian HIV, even when the scientists repeatedly exposed them to high levels of the virus over an eight-month period.
Lead study researcher Michael Farzan, an immunologist at the Scripps Research Institute, said, “Our compound is the broadest and most potent entry inhibitor described so far. Unlike antibodies, which fail to neutralize a large fraction of HIV-1 strains, our protein has been effective against all strains tested, raising the possibility it could offer an effective HIV vaccine alternative.”
Along with providing protection to the monkeys, the lab tests showed the drug candidate helped in blocking all the known strain of HIV-1 and HIV-2, which are the two main types of the AIDS virus that infect humans.
It was built on prior research works by Farzan’s lab into a receptor known as CCR5, which plays a key role in allowing the AIDS virus to latch onto a cell’s surface and start replicating.
The new compound of the drug binds to two sites on the virus’ surface at the same time, preventing the infection of a cell.
Hailing the results of the study, Farzan said, “This is the culmination of over a decade’s work on the biochemistry of how HIV enters cells. When we did our original work on CCR5, people thought it was interesting, but no one saw the therapeutic potential. That potential is starting to be realized now.”
The study was published in the journal Nature.