HIV in suicide mode! In a breakthrough, researchers, including an Indian origin scientist, have created a microbicide that can trick HIV into killing itself without disturbing any healthy cells.
Pinning down an effective way to combat the spread of the human immunodeficiency virus, the viral precursor to AIDS, has long been a challenge for scientists and physicians, because the virus is an elusive one that mutates frequently and, as a result, quickly becomes immune to medication.
A team of Drexel University researchers is trying to get one step ahead of the virus with a microbicide they've created that can trick HIV into "popping" itself into oblivion.
The microbicide DAVEI - which stands for "Dual Action Virolytic Entry Inhibitor" - is the latest in a new generation of HIV treatments that function by specifically destroying the virus without harming healthy cells, researchers said.
"While several molecules that destroy HIV have recently been announced, DAVEI is unique among them by virtue of its design, specificity and high potency," said Dr Cameron Abrams, a professor in Drexel's College of Engineering and a primary investigator of the project.
A team co-led by Abrams and Dr Irwin Chaiken in the Department of Biochemistry and Molecular Biology in Drexel's College of Medicine, and including R V Kalyana Sundaram, developed the chimeric recombinantly engineered protein - that is, a molecule assembled from pieces of other molecules and engineered for a specific purpose, in this case to fight HIV.
HIV invades a healthy cell by first attaching via protein "spikes" that then collapse to pull viral and cell membranes together, fusing them and allowing the genetic contents of the virus to enter the healthy cell.
The cell is rewired by the viral genetic material into producing more viruses instead of performing its normal function, which, in the case of cells infected by HIV, involves normal immunity. AIDS is the result.
"We hypothesised that an important role of the fusion machinery is to open the viral membrane when triggered, and it follows that a trigger didn't necessarily have to be a doomed cell," Abrams said.
"So we envisioned particular ways the components of the viral fusion machinery work and designed a molecule that would trigger it prematurely," Abrams said.
The team designed DAVEI from two main ingredients. One piece, called the Membrane Proximal External Region (MPER), is itself a small piece of the fusion machinery and interacts strongly with viral membranes.
The other piece, called cyanovirin, binds to the sugar coating of the protein spike. Working together, the MPER and cyanovirin in DAVEI "tweak" the fusion machinery in a way that mimics the forces it feels when attached to a cell.
The study was published in the journal Antimicrobial Agents and Chemotherapy.
