As researchers work to defeat HIV - the virus that causes AIDS - they have developed an ever-increasing number of medications. "But to date most of these rely on trying to cripple the virus or inhibit one of the viral proteins," explains Dr. Pamela Schwartzberg, a senior investigator at the National Genome Research Institute. And the problem with this approach, according to Schwartzberg, "is that because the virus rapidly mutates, those inhibitors are subject to the rapid development of resistance."
Her laboratory has been looking at T-cells ? the kind of white blood cells that HIV infects ? and at T-cell proteins. She says that there's been a growing interest in the idea of developing medications that target human cellular proteins, instead of those of the HIV virus. Some human proteins are used by HIV in its replication process, but Schwartzberg explains that T-cell proteins would be less prone to developing resistance to medications, because human proteins do not mutate as fast as viral proteins do.
Schwartzberg focused on a specific human T-cell protein called ITK. "What we found is that when we inhibit the function of this protein, or if we inhibit its expression, we find that it actually does block HIV infection." She explains that inhibiting ITK affects multiple stages of the HIV life cycle. "So in fact we think it's a very intriguing model for how you could use the cell to try to inhibit HIV replication as opposed to just blocking the virus."
Schwartzberg stresses that researchers are still a long way off from developing new HIV medications based on these findings. Her research was published in the April 28 online edition of the Proceedings of the National Academy of Sciences.