Prof. Gary Whittaker, assistant professor of microbiology and immunology, and Victor C. Chu grad have discovered a potential vulnerability in the influenza virus. They found a specific receptor that, if targeted, can prevent the virus from infecting new cells, regardless of its strain.
“This could lead to what I like to call a universal medication for influenza,” Whittaker said, explaining that antiviral drugs could be designed to specifically target the molecule or co-receptor that allows the virus to enter and infect cells. This medication, he said, would be different from vaccines in that, “With vaccines, we’re always one step behind the virus … we have to wait for it to arrive, then we can make the vaccine … it might be too late by the time we give it to people.”
Whittaker proposed that a technique of exclusion called a “ring vaccination” could be applied while using the medication. He explained that once a person is infected, all those in close contact with him would be given the medication in order to prevent an outbreak. Chu added that, although the influenza virus replicates very quickly upon entering a cell, the medication would be capable of preventing the virus from spreading out to infect other cells and other people. Whittaker estimated it would be at least nine years of clinical trials before such a medication could be used as common treatment, drawing a parallel with a similar discovery made in 1996 about the Human Immunodeficiency Virus (HIV). In that discovery, researchers also found a co-receptor that plays a similar role for HIV infections as this particular molecule does for the influenza virus.
Chu noted, “Personally, I think the best way to treat the flu is to develop vaccinations,” adding that they could be used in conjunction with antiviral treatments.
Whittaker explained that many assumptions have been made about the influenza virus, and that he and Chu reevaluated these assumptions to arrive at their discovery. Whittaker explained that during their research they considered the two possible targets: the virus itself, or the cell. While the virus itself mutates and changes, Whittaker pointed out that the cell is unlikely to change, and therefore targeting the cell would minimize the chances of the virus becoming resistant to possible antiviral treatments. Through their research, Whittaker and Chu noticed a molecule that they had “never realized was there before.” They suggested that without this surface molecule, known as N-linked glycoprotein, the virus would be able to attach itself to the cell, but not infect it.
Chu added that, when it came to targeting receptors, specificity was most important.
“The influenza virus is a carbohydrate or a sugar in the most basic sense,” he said. “That’s not specific at all…It would not make a good target.”
The significance of their discovery then, Chu concluded, was that they had found a protein base responsible for the infection process, which was far more specific a target than originally imagined.
While they have yet to identify the co-receptor responsible for this occurrence, Chu pointed out that the first step of realizing this critical component’s existence is significant in and of itself, and that their work would continue in hopes of identifying the co-receptor in question.
Whittaker and Chu’s findings were published in the Proceedings of the National Academy of Sciences (PNAS) in December.
Archived article by Julie Geng
Sun Staff Writer