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Clients in the News – University of California Researchers open door to new HIV therapy

The AIDS virus enters immune cells by binding to CD4 receptors embedded in the membrane (parallel lines) of the cell. But once a virus enters the cell, it makes a protein, Nef, that binds to the protein complex underlying CD4, tagging it for the waste bin. Potential anti-HIV drugs would disable one of the proteins (colored blobs) to which Nef binds, interfering with HIV’s strategy for spreading through the body.
Credit: Image by James Hurley, UC Berkeley

People infected with the Human Immunodeficiency Virus (HIV) can stave off the symptoms of AIDS thanks to drug cocktails that mainly target three enzymes produced by the virus, but resistant strains pop up periodically that threaten to thwart these drug combos.

Researchers at the University of California, Berkeley, and the National Institutes of Health have instead focused on a fourth protein, Nef, that hijacks host proteins and is essential to HIV’s lethality. The researchers have captured a high-resolution snapshot of Nef bound with a main host protein, and discovered a portion of the host protein that will make a promising target for the next-generation of anti-HIV drugs. By blocking the part of a key host protein to which Nef binds, it may be possible to slow or stop HIV.

“We have imaged the molecular details for the first time,” said structural biologist James H. Hurley, UC Berkeley professor of molecular and cell biology. “Having these details in hand puts us in striking distance of designing drugs to block the binding site and, in doing so, block HIV infectivity.”

Hurley, cell biologist Juan Bonifacino of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) of the National Institutes of Health and their colleagues report their findings in a paper published today (Jan. 28) by the open-access, online journal eLife.

The report comes a month after President Barack Obama pledged to redirect $100 million in the NIH budget to accelerate development of a cure for AIDS, though therapies to halt the symptoms of AIDS will remain necessary for the immediate future, Bonifacino said.

“For many patients, current drug therapies have transformed HIV infection into a chronic condition that doesn’t lead to AIDS, but anything we can develop to further interfere with replication and propagation of the virus would help keep it in check until we find a way to completely eliminate the virus from the body,” he said.

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