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A newly published AIDS study could open another front in the battle against HIV infection by showing that gene therapy can be used to stop infected cells from spreading the deadly virus, researchers said.
In a test-tube experiment believed to be the first of its kind, researchers based at Children’s Hospital of Philadelphia were able to block the operation of the "tat" gene that allows HIV to spread throughout the body from infected cells.
Up to now, genetic AIDS research has concentrated on finding ways to help healthy cells withstand the ravages of the HIV virus that infects an estimated 16,000 new victims a day, mainly in the developing world.
But by working with human cells already infected with HIV, the team was able to reduce the tat gene’s virus-replicating functions by 80 percent to 90 percent, according to findings published in the journal Gene Therapy.
That, researchers said, raises the possibility of a new gene therapy approach capable of supplementing the current drug-based treatment known as highly active antiretroviral therapy, or HAART, which is used to stop HIV infection from becoming full-blown AIDS.
In recent studies, HAART has proved to be a costly drug regimen that poses serious side effects for HIV patients while delivering questionable results.
"This is proof of the concept that HIV replication could be inhibited by a genetic approach, though we’re not at 100 percent yet," said Dr. Stuart Starr, a study coauthor and chief of immunologic infectious diseases at Children’s Hospital.
"Everyone thinks of an antiviral approach, or an immunologic approach (to HIV). This adds another option into the equation that could become more important as other options prove not to be totally successful."
Key to the study was an artificially produced "antitat" gene provided by the Washingtonbased Research Institute for Genetic and Human Therapy.
Children’s Hospital researchers used a mouse retrovirus to deliver the antitat gene into HIV-infected U-1 and ACH-2 cells, which were developed in the lab from the tissues of living HIV patients.
They found that when the antitat protein combined with the tat gene, it successfully inhibited the gene’s operation without disturbing healthy cells or causing toxic side-effects.
The study, funded by a private foundation, also found that the introduction of the antitat gene prolonged the survival of immune-system cells called CD4+T lymphocytes.
Starr said researchers have entered preliminary discussions with a New England-based primate center, where animal experiments could be carried out on infected macaque monkeys.
If animal experiments proved successful, the Children’s Hospital team would hope to have a gene therapy treatment ready for human clinical trials in three to four years.
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