The findings show that the introduction of a harmless molecule that uses the same machinery a virus needs to grow may be a potent way to shut down the virus before it infects other cells or becomes resistant to drugs. The results are published in the March issue of the journal, Antimicrobial Agents and Chemotherapy.
"When a virus encounters a susceptible cell, it enters and says, 'I'm now the boss,'" explains John Yin, a UW-Madison associate professor of chemical and biological engineering and senior author of the paper. "It pirates the cell's resources to produce virus progeny that, following release from the host cell, can infect other cells."
The current technique to stop a virus in its tracks is to develop drugs that bind to and block the function of virus proteins - molecules the virus produces, with the aid of host cells that help the virus replicate, or make copies of itself. The drugs, says Yin, are like hammers that knock out key functions that the virus uses for growth and reproduction.
But, he points out, this antiviral approach cannot always outsmart the virus: "When a virus reproduces, it doesn't do so perfectly. Sometimes, it inserts genetic typos, creating variations that may allow some versions of the virus proteins to develop an evolutionary advantage, such as drug resistance."
While improvements in molecular biology and chemistry have led to new drugs that precisely target virus proteins, they have not been able to stop viruses from producing drug-resistant strains.
"Despite advances in the development of antiviral therapies over the last decade, the emergence and outgrowth of drug-resistant virus strains remains problematic," says Hwijin Kim, a UW-Madison graduate student in the chemical and biological engineering departmen