The research team at the MRC ™s National Institute for Medical Research pinpointed crucial differences in a gene found in rhesus monkeys that can prevent HIV infection, and its human counterpart, that cannot.

The differences indicate that HIV infection would not have become established in the human population if the form of the gene present in certain monkeys had also been present in humans. More importantly, the studies reveal that only a single change to the human gene is needed to enable it to interfere with the replication process of the HIV virus and prevent infection.

Lead scientist, Dr Jonathan Stoye, said:

This discovery has significant implications for the development of effective gene therapy to combat AIDS.

In theory, it should be possible to take cells from an HIV-infected individual, make them resistant to HIV infection with the modified gene and reintroduce them into the patient. These cells could then block progression to AIDS.

Alternatively we could seek for drugs that activate the human gene against HIV.

The research findings are published in full in this week ™s edition of Current Biology.

According to the latest UNAIDS figures, at the end of 2004, 39.4 million people worldwide “ 37.2 million adults and 2.2 million children younger than 15 years “ are living with HIV/AIDS.

HIV stands for 'human immunodeficiency virus'. HIV is a retrovirus that infects cells of the human immune system and destroys or impairs their function. Infection with this virus results in the progressive depletion of the immune system, leading to 'immune deficiency', or AIDS. AIDS stands for 'acquired immunodeficiency syndrome' and describes the collection of symptoms and infections associated with acquired deficiency of the immune system.

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Flurizan is currently being studied in a Phase 2 clinical study in approximately 210 patients with mild to moderate Alzheimer's disease. All patients have now been on drug for more than 9 months. The trial's Data Safety Monitoring Board has reviewed safety data from the trial each calendar quarterly and has determined that the trial should proceed without change. This Phase 2 trial is expected to conclude its clinical study period in March of 2005.

Flurizan has been shown to modulate gamma-secretase and selectively lower levels of Amyloid beta 42, a toxic peptide that is believed to be a chief culprit in the cause of Alzheimer's disease. In transgenic mouse studies, Flurizan has demonstrated the ability to reduce brain amyloid levels and prevent memory loss. Flurizan was selected during preclinical testing to avoid cyclooxygenase inhibition and its related side effects.

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