Scientists Spot New Twist in HIV Infection

Discovery brings better treatments, even a cure, a bit closer

By E.J. Mundell
HealthDay Reporter

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THURSDAY, Sept. 4 (HealthDay News) -- The virus that causes AIDS infects one form of immune T-cell by rearranging its inner skeleton, allowing it access to the cell, scientists have discovered.

The finding helps explain how HIV maintains pockets of dormant virus in these so-called "resting" T-cells, even when the virus is under attack by antiretroviral drugs. It also points to potential new targets for drug development, experts say.

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"Whenever you identify a necessary step -- a step which is absolutely required for infection of naive T-cells -- of course then you have a new focus point, one that you can examine to see if there are options for new therapies. Certainly with HIV treatment, we need that," said study co-author Jon Marsh, a researcher in the Laboratory of Cellular and Molecular Regulation at the U.S. National Institute of Mental Health.

Viruses are such primitive life forms that they must gain access to other organisms' genetic material, located deep in the nucleus of the cell, before they can replicate. Scientists have long known that HIV latches onto certain receptors on the surface of its main target -- the immune system's T-cells -- to gain entry into the cell.

Early in the disease process, HIV typically attacks "activated" T-cells -- so named because they are already primed against a particular pathogen. But so-called "naive" T-cells also move throughout the bloodstream. These cells are often resting -- they haven't yet been activated to fight a particular threat.

When HIV seeks entry to the activated T-cell, it does so by latching onto a surface receptor called CCR5. But in more than 50 percent of patients, the virus begins to attack resting T-cells, too, via a receptor called CXCR4.

"We know that HIV prefers to infect activated T-cells -- it's more difficult for HIV to infect resting T-cells," noted Rowena Johnston, vice president of research at the Foundation for AIDS Research (amfAR) in New York City. "So, the question for me and a lot of people has been: Why does the virus do it? What possible advantage could there be?"

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