Research points to cheaper Aids drugs

By MARTIN JOHNSTON, health reporter

New Zealand scientists will today unveil preliminary research which could lead to a new class of drugs to attack HIV/Aids.

Their investigation centres on the way human cells "read" viruses such as HIV.

Professor Warren Tate and colleagues from Otago University have shown that for a virus to reproduce itself in the body, its genetic material must be "read" in a particular way by human cells.

Interrupting that process could be the key to opening a newfront against HIV by developinga new class of drugs.

More than 800 people in New Zealand and about 40 million worldwide have HIV/Aids.

Professor Tate will present his research to the Pacific Rim Biotechnology Conference in Auckland today.

He said test-tube trials involving extracts of rabbit cells had already produced promising results. Two chemical compounds derived from existing antibiotics were involved.

Similar trials were under way to test 30 to 40 more compounds.

If a drug proved successful, it would add dramatically to the pharmaceutical attack on HIV, but any human trials would be years away.

Modern drugs control the disease in many people, but problems remain: there can be severe side-effects, the virus is developing resistance to some drugs and many are too expensive for Third World countries, including those in Africa, where the epidemic is worst.

In New Zealand, drugs can cost $1200 to $1600 a month per patient.

Professor Tate said his team was using low concentrations of active chemicals in the drugs it was testing.

This put them below the level that caused side-effects and would, he hoped, make them cheap enough for the Third World.

His group - some of whom were applying the same findings to hepatitis B - was one of few in the world investigating this virus-reading mechanism of human cells.

"For many people ... it's just too out-in-left-field to even contemplate. In some ways, that's why it provides us an opportunity in a niche way to try and exploit this.

"I stumbled upon this mechanism in collaboration with an American group first in the mid-1980s in a bacterial gene."

Others later found it also operated with a particular infection in chickens and then with HIV in humans.

The way in which human immune cells read the genetic code of HIV allows the virus to make two proteins, one for its viral coat and one for replication in the exact proportions needed.

"That's critically important for infection with the virus to continue."

If scientists could disturb those proportions enough, HIV's infection capability would drop dramatically.

An Auckland Hospital infectious diseases specialist, Dr Mark Thomas, said the Otago approach sounded as if it would alter the way the virus used the cell as its factory to produce more viruses.

The team is receiving nearly $1 million over three years from the Health Research Council.

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