A protein being developed by Sangamo BioSciences Inc. appeared in laboratory testing to make human immune system cells permanently resistant to HIV infection, the company said on Wednesday.

Previously, the company had demonstrated only short-term resistance, said company spokeswoman Elizabeth Wolffe.

Sangamo said cells modified with its protein, a zinc finger DNA-binding protein nuclease, survived continuous exposure to HIV, the virus that causes AIDS, and expanded to the point that they represented the vast majority of cells at the end of the 70-day experiment.

Shares of Sangamo, which rose 5.1 percent to close at $5.38 on Nasdaq, were up another 17 percent at $6.30 in after-hours trading.

"We have now shown that we can get permanent modification and permanent HIV resistance," Wolffe said.

She also said the company has not changed its goal of launching a human clinical trial this year, but did say that "there are more experiments that have to be done."

The Sangamo compound is part of a newly evolving class of drugs known as CCR5 receptor antagonists, which target a strain of the HIV virus called R5 and are designed to block a key receptor needed by the virus to enter and infect the cell. Current treatments work by preventing the virus from replicating once it is inside the cell.

GlaxoSmithKline Plc terminated a CCR5 program because of liver toxicity, while Schering-Plough Corp. discontinued a trial after patients experienced sharp spikes in the amount of the HIV virus in their blood.

 

Measuring the amount of AIDS virus circulating in the blood of HIV-positive patients is not a good indicator of the health of their immune systems, researchers said on Tuesday.

Physicians often assess the amount of HIV particles in the blood -- known as the viral load -- along with the decline in CD4 cells that help the body fight infections to measure the disease's progress and decide when to prescribe drug therapy.

But a study of 2,800 untreated HIV-positive individuals found only about 5 percent of the variations in viral load corresponded to variations in immune system damage.

Depletion of CD4 cells is therefore not a simple consequence of the amount of virus circulating, said the study published in this week's Journal of the American Medical Association.

"The results of this nationwide study may have profound implications in our understanding of how HIV causes disease and in our approach to the management of HIV-infected patients," said lead investigator Dr. Benigno Rodriguez of Case Western Reserve University in Cleveland.

Estimating damage to the immune system is critical in deciding when it is best to start antiretroviral therapy, the AIDS-fighting drugs credited with allowing millions of infected people to live with the disease.

Because of issues of drug resistance and the potent side effects of the drugs, doctors and patients often defer starting medications until medically necessary.

The study challenges the current belief that the degree to which the virus replicates itself is the trigger for the loss of CD4 cells, white blood cells that are a key component of the body's immune system.

An accompanying editorial in the journal said the findings were exciting because they suggested that researchers should look for and target non-viral factors that set off the eventual decline in the immune system.

Bristol-Myers Squibb Co. and Gilead Sciences Inc. said on Thursday they have reached agreement to commercialize a three-in-one AIDS pill in Canada.

ATRIPLA won U.S. approval in July, the companies said on Thursday.

The drug is the first ever once-daily drug for adults with HIV, which causes AIDS. The pill contains Bristol's drug Sustiva and Gilead's medicines Viread and Emtriva.

The companies will work together to win regulatory approval in Canada and will share responsibility for commercializing the drug once it is approved, they said.