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Page: << Prev | 1 | 2 | 3 | Next >> An activated T-cell is the ideal host for HIV, Schwartzberg pointed out, and ITK appears to be crucial to HIV's invasion and spread.
"We found that there were several cellular processes in T-cells that HIV needs to use and that ITK was important to," she said. "In fact, it seems to affect three stages in the HIV life cycle. That was a real surprise to us."
But would inhibiting ITK inhibit HIV? The researchers got help in answering that question from the pharmaceutical industry, which has been developing ITK inhibitor drugs as possible anti-asthma medications.
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In laboratory experiments, Schwartzberg and Henderson used these experimental ITK inhibitors -- as well as another technique, called RNA interference -- to reduce ITK activity in HIV-infected T-cells.
"We could see rather dramatic effects on HIV replication in T-cells," Schwartzberg said.
Without active ITK in host T-cells, HIV found it much harder to enter the cell and to transcribe its genetic material into new viral particles, the team found. "The effect was quite strong over the course of a week, which was the length of time that we looked at," Schwartzberg said.
Of course, ITK is important to the proper function of immune T-cells, so questions remain as to whether its suppression might have unwanted side effects, such as a weakening of immune function. But experiments in mice suggest these effects might be minimal.
ITK-suppressed mice did have impaired immune function, but it was mostly confined to a specific type of response -- the defense the body mounts against allergies and asthma, Schwartzberg said. In other respects, ITK-suppressed cells appeared to "function in many circumstances, and they can fight off many infections," she noted.
Still, it's a long way from research in the test tube and in mice to human clinical trials. But the promise of a human cell-based HIV medication that attacks the virus at three different spots in its life cycle is hugely attractive, Johnston said.
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