Attacking at the vulnerable point

Attacking at the vulnerable point

Paradoxically, HIV is at its most vulnerable when it is replicating, and that is when the drugs can work.

"The drugs work on their enzymes, or bits of the virus that help it replicate. The drugs currently don't work on those bits of virus stuck into the host DNA," Professor Lewin said.

To move towards curing HIV or getting closer to a cure, drugs have to attack the latent cells - the ones holding the HIV virus in their DNA.

While HIV can hide in a variety of cells, the ones Professor Lewin's team targets are white blood cells, also called T cells, which are the cells which HIV preferentially attacks, causing its terrible immune deficiency.

When the human body is infected with a virus, the lymphocytes, or T cells, get a wake-up call to action, and once they have done their job they go 'back to sleep'.

From studies involving monkeys, it looks as though HIV integrates with the cells' DNA while the cells are resting.

Despite these studies, so far scientists have not even been able to imitate latency in the laboratory, so they can study how to interfere with it.

But Professor Lewin's team has made a breakthrough.

"What we've been doing is trying to mimic what happens in the tissue or in a person's body to allow infection of resting cells," she said.

"We focused on a particular protein or something called a chemokine, which is a protein that directs cells around the body, it's like a chemical messenger.

"We began thinking, maybe it was these chemokines that were conditioning resting cells to become infected."