New research shines light on combating HIV

HIV

HIV

A  recent study conducted by Drexel University researchers discovered a way to “trick” the human immunodeficiency virus into killing itself, a potentially critical discovery to combating the virus responsible for AIDS.

The study was co-led by Dr. Cameron Abrams, a professor at Drexel’s College of Engineering, and Dr. Irwin Chaiken of Drexel’s College of Medicine’s Department of Biochemistry and Molecular Biology. The research team, which also included Dr. Mark Contarino and doctoral students Arangassery Rosemary Bastian and R. V. Kalyana Sundaram, developed a protein to fight against HIV; the study findings will be published in October’s issue of the American Society for Microbiology’s journal, Antimicrobial Agents and Chemotherapy.

The protein, which was engineered by piecing together different molecules, is called a “Dual Action Virolytic Entry Inhibitor.” Preclinical research studies showed the molecule can cause the HIV virus to destroy itself without harming healthy cells.

The molecule works by altering the HIV’s ability to conduct fusion machinery, a mechanism by which HIV attaches itself to a healthy cell.

“We hypothesized 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.”

The molecule, composed of a Membrane Proximal External Region and a cyanovirin, change the fusion machinery to cause the HIV to release its poison before it attaches to a cell, causing the cell to die without harming healthy cells.

“DAVEI and other new-generation virolytic inactivators open up an important opportunity to develop a topical microbicide to block the transmission of HIV, and at the same time provide lead ideas to discover treatment strategies for people who are already infected,” Chaiken said. “Our hope is that determining the structural driving forces of both inhibitors and viral entry machinery that enable spike inactivation will help to advance molecular designs with increased power, specificity and clinical potential for both prevention and treatment.”

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