Stopping virus replication

Stopping virus replication

The chemokines call the white blood cells, or T cells, to respond to the invasion of a disease by moving to a lymph node, where they can give the best response.

Professor Lewin's team discovered that while the T cells were still travelling around the body, or 'resting', they could be infected with the HIV virus and become latent.

"We did a pretty simple experiment, we just took resting T cells from blood donors, and we incubated those T cells with these chemokines, and then tried to infect the cells," she said.

"What we found was we could establish latency in the test tube. We got infection, we got integration, and then the cell just sat there, it didn't start pumping out the virus."

Without the chemokines to call them back to the lymph glands, the T cells could not be infected.

When the T cells were in the lymph glands but still in their 'resting' state, they could become infected, but the HIV virus could not integrate with the cell's DNA and therefore could not replicate itself.

"So in fact in an unactivated resting cell, HIV would enter, will start trying to replicate, but it can't get into the nucleus, it can't get into the DNA," she said.

"But we've shown that if we tickle them up with these chemokines, we get very good, high levels of HIV integration."

This means Australian scientists now have a base from which to study latency in the laboratory, which may lead to a way to stop HIV from replicating itself.

Blocking the chemokines from calling T cells back to the lymph glands is not an option because it would damage the immune system, but scientists may find another way to combat the virus.

"There are a whole lot of things we want to do now," Professor Lewin said.

"We want to understand how those chemokines change the cell, which would allow efficient entry and integration.

"We think that's a really good model to test new drugs that could potentially target latency."