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Back To Vidyya A Look At New AIDS Drugs Under Development

Hope Is Always On the Horizon

An entirely new class of AIDS drugs on the horizon may offer just-in-time help to many patients whose treatment options are running out, researchers said Thursday.

The latest data suggest these drugs may dramatically restore health - at least temporarily - to people dying because the virus has grown resistant to all the currently available AIDS medicines.

The new drugs block HIV in a different way from the standard medicines that have revolutionized AIDS treatment in recent years. Instead of gumming up the virus's ability to manufacture new copies of itself, they block the virus from getting inside blood cells.

The drugs are called entry inhibitors and are being developed by many companies, although only one has entered broad human testing.

"They hold significant promise for the treatment of HIV," said Dr. Joseph Eron of the University of North Carolina.

Doctors discussed the drugs at the 13th International AIDS Conference, where the latest data were presented on Trimeris, Inc.'s experimental T-20, the most advanced medicine in the field.

Combinations of drugs introduced about five years ago turned AIDS from a death sentence to a treatable disease, at least in parts of the world where people can afford the medicines. These combinations can drive the virus below detectable levels, but in about half of patients, the virus returns within a year.

When this happens, doctors switch their patients to different combinations of the 14 available drugs. However, the virus usually returns even more quickly with each new drug cocktail.

Most of these people remain outwardly well, despite their virus levels. But no one knows how long this will last, and doctors worry they will be left with nothing to fight the disease.

"We desperately need new targets for tackling HIV," said Dr. Julio Montaner of the University of British Columbia. "We think these people will need help in the not too distant future."

The current drugs fit into three major classes. But all work by blocking the virus's ability to make new copies of itself once it infects a cell. The new drugs instead are designed to stop the virus from penetrating cells to start this process.

When the new drugs are used alone, the virus appears to quickly grow resistant to them, just as it does with other medicines. So doctors envision combining these so-called entry inhibitors with the standard medicines to keep a step ahead of the virus.

"Drugs that work on the outside of the cell would be a tremendous addition to the drugs that work on the inside," said Dr. David Ho of the Aaron Diamond AIDS Research Center in New York City.

Dr. Cal Cohen of the Community Research Initiative of New England presented data on 71 patients who took T-20 after failing with all the standard drugs. Fourteen did not get better, and 16 others dropped out of the study for a variety of personal reasons. But after one year, 41 are still in the study and responding well to the treatment.

Their average virus levels were 100,000 copies per milliliter of blood before treatment and 3,000 copies now.

Among the patients was a dying man, blind in one eye from an AIDS-related infection, whose HIV-ravaged white blood cells had dropped to a precipitous 33 copies per cubic millimeter of blood. After a year on T-20 and four standard AIDS drugs, his blood cells have risen to 430 copies, and his virus level is barely detectable.

"Now he is even healthier looking than I am," Cohen said. "He's back to life. You control the virus, and good things happen."

The drug's major drawback is that it must be injected twice a day, but Cohen said patients seemed able to do this without difficulty.

Fusion inhibitors, plus new versions of standard drugs, "may be exactly what people need," Cohen said.

Trimeris is designing large, final-stage testing of T-20. Officials say this will involve people at earlier stages of infection.

In recent years, scientists have worked out the mechanics of the devilishly sophisticated process by which the virus gets into its targets. T-20 works by blocking one step in the fusion of the virus to cells, and other drugs interrupt at other points.

Another of these entry-blocking drugs, developed by Schering Plough, begins first-stage human testing this month in the United States.

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Editor: Susan K. Boyer, RN
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