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Turning promise into HIV therapy

The Human Immunodeficiency Virus (HIV) is a nasty bug. Being little more than genetic material with protective coating around it, all viruses rely on hijacking their hapless host cells’ molecular machinery in order to reproduce. HIV’s target is a type of T-cell in the human body that plays a key role in mounting an effective immune response to invading pathogens. As more of these T-cells fall victim to HIV, the person infected by the virus becomes less able to fend off other diseases, such as tuberculosis, and develops AIDS. Current drug therapy tries to protect the immune system by limiting HIV replication. These days, with the help of such anti-viral drugs, HIV-infected people are able to lead a normal life. But the drugs are not able to flush out the virus completely from the body and the infected people must take the medication every day for the rest of their lives. The reason why HIV is so hard to eradicate from the body is that it integrates its own genes into the genome of the T-cells it infects. If infected cells divide, the daughter cells automatically inherit the viral genome as well. Worse, the anti-viral drugs cannot deal with infected T-cells that go into a dormant state. Now, in a paper published in the journal Science, an Indian researcher and her scientist colleagues in Germany have shown that it might be possible to remove entirely the viral genome from the infected cells. Working with cultured cells, the scientists have demonstrated that an enzyme can be created to recognise and excise only the viral genetic sequences from the genome of infected cells. “The results,” notes a commentary in the journal, “raise the possibility that customised enzymes might some day help to eradicate HIV-1 from the body.”

The research opens up a whole new approach towards creating more effective anti-HIV drugs. But it will be naive to conclude that better therapy based on this technique, not to mention a cure for HIV, is round the corner. For one thing, the method must be shown to work with infected T-cells. Then the technique must be translated into one that can be used on model animals, which will bring its own share of problems. As Indrani Sarkar, first author of the Science paper, points out, th e biggest challenge will be a delivery system “to make sure that the enzyme reaches the [viral genetic] sequences we intend it to reach.” She believes that a minimum of 10 years of further research will be needed before clinical trials can even be contemplated. As the pharmaceutical industry knows only too well, many approaches look promising at the lab level but only a few make it to clinical trials and still fewer reach regular medical use. The new proof-of-concept method published in Science needs to go a long way before it can even aspire to become mainstream therapy.

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