New approach flushes out hidden HIV
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A strategy used by the wily AIDS virus to perpetuate infection may be susceptible to attack, according to a new report.
One of the fundamental difficulties in trying to eradicate HIV in people infected with the virus is that, even with the best antiviral treatment, small numbers of the virus can lie dormant in immune cells, ready to break out and multiply rapidly when the opportunity occurs.
This week, researchers report a way to flush the latent virus out of its hiding place in resting CD4 cells (immune cells that have not been activated to fight off microbes), and then pick it off with potent drugs.
The weapon that exposes the hidden virus is a drug that’s commonly used to treat bipolar disorder—valproic acid. According to results of a proof-of-concept study, treatment of HIV-infected patients with valproic acid, along with intensified ‘HAART’ (highly active antiretroviral therapy) seems to accelerate clearance of replication-competent HIV.
Dr. David M. Margolis, from the University of Texas Southwestern Medical Center at Dallas, and his associates report their results in this week’s Lancet medical journal.
The researchers noted that valproic acid inhibits an enzyme called HDAC1, which is responsible for enabling HIV to remain latent inside cells. “We know that in model systems in the laboratory, isolating resting cells from patients and incubating them with valproic acid induces expression of virus,” Margolis explained in an interview with Reuters Health.
For their current study, Margolis and his colleagues worked with four HIV-infected volunteers who were taking HAART and had very low viral levels for more than 2 years. The researchers intensified HAART treatment by adding the relatively new fusion inhibitor enfuvirtide (a.k.a., T-20), and then had the subjects take valproic acid, 500 to 750 milligrams twice daily, for 3 months.
“We then found a significant decrease in the amount of recoverable virus and the amount of cells that could express replication-competent virus,” Margolis said. Specifically, the frequency of infection in resting CD4 cells declined in all four patients, and to a significant extent in three of them..
He added, however, that this short-term treatment did not result in cure for any of the subjects, and that further research will be required to confirm these results and to test the efficacy of longer-term HDAC1 inhibition.
“These results, though preliminary, merit further urgent study,” Dr. Jean-Pierre Routy, from McGill University Health Centre in Montreal, asserts in a related editorial.
“This is the first glimpse of a new therapeutic approach that might represent a possible step towards making HIV-infection no longer a chronic disease,” he writes
SOURCE: Lancet, August 13, 2005.
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