Oct. 30 (Bloomberg) -- Antibodies derived from the blood of HIV-infected people suppressed the virus in the blood of monkeys in two studies that suggest the experimental approach may improve AIDS therapy or point the way toward a cure.
One study showed that a single injection of antibodies reduced the simian, or monkey, version of HIV to undetectable levels in three to seven days -- much faster than regular AIDS drugs -- and the effect lasted for almost two months. The research, led by Dan Barouch, professor of medicine at Harvard Medical School, is published today online by the journal Nature.
The antibodies represent a new and potentially more powerful approach to treating a disease currently controlled by daily pills such as those made by Gilead Sciences Inc. While those drugs have transformed HIV from a death sentence into a manageable disease, they don’t completely clear the virus from the body. The new antibodies attack HIV in areas the drugs don’t reach, suggesting they may have a role in curing a disease that has confounded scientists for 30 years.
“The antibodies themselves are very, very special,” said Barouch, director of the Center for Virology and Vaccine Research at Beth Israel Deaconess Medical Center, a Harvard affiliate in Boston. “These antibodies should be explored for a variety of different clinical applications. Clearly where there’s going to be substantial interest is evaluating their potential role in cure.”
The virus came back in most of the monkeys as expected as levels of the antibodies waned. In three animals, however, the virus still hasn’t rebounded, suggesting the treatment may have kept it in check without further help.
That indicates the antibodies are replicating a rare phenomenon in a group of HIV-infected people called elite controllers whose immune systems keep the virus at bay without the daily pills that are a lifeline for most patients.
“We’re not saying those animals are cured,” Barouch said today in a telephone interview. “It looks like we did convert those animals into elite controllers.”
Barouch and colleagues are in discussions with drugmakers over plans to test the antibodies in humans, though no agreement has been reached, he said, adding he can’t disclose details of the plans. “There is serious interest from industry,” Barouch said.
HIV does its damage by hijacking immune-system cells and using their machinery to replicate itself. While pills such as Gilead’s Atripla block the replication process, they don’t directly target the virus as it moves through blood, and don’t kill infected cells. The new antibodies achieve both targets.
The second study, led by Masashi Shingai at the U.S. National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, found a similar result. The group tested two antibodies separately, but found they only suppressed the virus for a week or less, leading to the development of resistant strains. Used together, the effect lasted as long as five weeks. When the virus eventually rebounded, a second dose brought it back under control.
“The findings of these two papers could revolutionize efforts to cure HIV,” Louis Picker, from Oregon Health & Science University, and Steven Deeks, of the University of California at San Francisco, wrote in an editorial accompanying the studies. They weren’t involved in the research.
To contact the reporter on this story: Simeon Bennett in Singapore at email@example.com