A nucleic acid, 2-5AN6B inhibited HIV replication in white blood cells from a group of 18 HIV infected patients by up to 80 percent, regardless of the patients’ treatment regimens.
"A cure for HIV infection remains an elusive goal despite the significant impact of current treatments because of the virus’ ability to adapt to and resist those treatments, and bypass the immune system’s natural defenses," said Robert J. Suhadolnik, Ph.D., prinicipal investigator and professor of biochemistry at Temple University School of Medicine. "This compound prompts the body to restore its natural antiviral defense systems against the invading virus."
Current drugs for HIV work by blocking one of the steps toward virus replication.
"This new anti-HIV compound works by a very different mechanism, and would appear to offer the promise of someday being combined with existing anti-viral therapies for a much more effective treatment. It is also very important that this compound is much less likely to be defeated by the ability of the virus to mutate, a problem often encountered with existing anti-viral drugs," said Thomas Rogers, Ph.D., co-author and professor of pharmacology at Temple.
This work builds on decades of research by the Temple team which was recently awarded a grant from the National Institutes of Health to continue pre-clinical studies on a larger scale. They’ll be investigating the molecular mechanisms of 2-5AN6B as a potential weapon against HIV, and continue work on a new therapeutic approach involving gene therapy for the treatment of HIV infection.
Eryn Jelesiewicz | EurekAlert!
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