Scientists have known since the 1980s that a small protein known as Vif plays an integral role in ensuring replication of the human immunodeficiency virus, HIV. To get a better idea of what Vif does, Michael Malim of King's College London and colleagues studied immune system T-cells infected with a form of HIV that lacked Vif. The team discovered that when the protein was absent, the T-cells were able to protect themselves from the virus. Specifically, the gene CEM15 seemed to interfere with the virus's lifecycle, rendering subsequent generations harmless.
The results point to new targets for pharmaceuticals. "If we can find a way to block the action of Vif," Malim says, "it would allow CEM15 to work properly and prevent HIV from spreading." Still, a lot about Vif remains unknown. Further clarification of its exact course of action, as well as identification of substances that can bind to and inhibit the protein within cells will be required before new drugs can be developed. "It's very ambitious," Malim notes, "but we may see Vif developed as a new target for therapy within the next ten years."