MU professor leads development of new HIV treatment
The drug shows promise to be stronger and longer-lasting.
Published Jan. 29, 2010
An MU researcher is part of a team developing a more potent and longer-lasting treatment for HIV, according to an MU news release.
The new compound, called EFdA, is 60,000 times more potent than existing HIV treatments and remains effective longer, said Stefanos Sarafianos, assistant professor of molecular microbiology and immunology in the School of Medicine and the researcher leading the MU team.
Sarafianos is collaborating with researchers from the University of Pittsburgh and the National Institutes of Health. Tests show EFdA also protects cells from HIV and shows potential for use in a vaginal cream to prevent HIV.
"The protection provided by EFdA is longer than by microbicides already in clinical trials," Sarafianos said.
The compound's effectiveness is due in large part to its unique chemical structure, said Michael Parniak, professor of biochemistry at the University of Pittsburgh School of Medicine.
EFdA is a nucleoside reverse transcriptase inhibitor, which inhibits the operation of reverse transcriptase, an enzyme needed for HIV to duplicate its DNA and spread.
EFdA has a chemical structure similar to that of a chemical essential to HIV for DNA synthesis that is missing in other NRTIs. Because EFdA has this structure, the HIV virus recognizes and incorporates EFdA into its own DNA and inhibits the virus's spread more efficiently than other anti-viral drugs do.
"The combination of the fact that EFdA is recognized so readily and activated so readily, plus the fact that it's very potent against the target, makes it overall so much better than anything that's out there right now," Parniak said.
The researchers also found EFdA was effective against HIV strains that are resistant to existing drugs, and they expect it will take longer for viral strains to become resistant to it.
"HIV will develop resistance to pretty much any drug you throw at it, but the time to resistance will vary depending on the drug," Parniak said. "And it looks to us like the development of resistance to EFdA will take a lot longer than to any other existing therapeutic that's out there."
In tests on monkeys with simian immunodeficiency virus, similar to HIV, EFdA proved 50 times as effective in inhibiting virus replication as other drugs. If the FDA approves EFdA, Parniak anticipates it to have a great impact on AIDS patients.
"It will be easy to take, because you need much less of this material than of existing drugs in order for it to have efficacy in the context of an infected organism," Parniak said. "And so that the chances of toxicity, which is the big issue with the current therapies, as patients have to take the drugs daily they eventually develop toxic responses, the side-effects that are associated with drugs. The fact that I think we'll have to use much less of EFdA than what's necessary of the current drugs would minimize the potential for toxicity."