Study shows anti-virals battle HIV via mutational meltdown

A new spectroscopy method has shed light on how special anti-viral drugs conquer certain diseases by inducing lethal mutation levels in pathogens. | Courtesy of
Researchers from the Massachusetts Institute of Technology (MIT) and the University of Chicago recently created a spectroscopy method that illustrates how anti-HIV drugs provoke lethal mutations within HIV’s genetic material, a discovery that sheds light on a process that has been poorly understood in the past and may improve attempts to create novel anti-viral treatments.

Viruses use rapid mutations to escape death in stressful environments, enabling them to become resistant to drugs. To counteract this strategy, scientists have developed lethal mutagenesis, a therapeutic anti-viral agent for various virus infections, such as Hepatitis C, HIV and influenza.

Lethal mutagenesis kills viruses by forcing them to mutate themselves to death. Viruses already have a high mutation rate, but the therapeutic treatments push that rate past its threshold. When viruses mutate too many times, they can no longer adequately manage their genetic material.

"They can't replicate and so are quickly eliminated," the University of Chicago's Gale Distinguished Service Professor in Chemistry Andrei Tokmakoff said. "In order to make this work, you need a stealth mutagen. You need something sneaky, something that the virus isn't going to recognize as a problem."

Study co-author John Essigmann, MIT's Leitch Professor of Chemistry, Toxicology and Biological Engineering, said two-dimensional infrared spectroscopy will be critical in continuing research.

"It lets us look at the structures that exist in aqueous solution, which is the natural milieu of cells," Essigmann said. "We also have done nuclear magnetic resonance, which is very informative, but those studies were done in organic solvents that probably do not as accurately provide a view of what happens in cells as did the infrared studies done by the Tokmakoff group.”

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