A New Potential Weapon Against the Flu That Isn't a Vaccine
Researchers at Ohio State University (OSU) are working on a potential new method of flu prevention that manipulates a natural process in the body—and isn't a vaccine. The study, published in PLOS Pathogens, focuses on a protein found naturally in the cells that helps fight viral infections, called IFITM3 (interferon-induced transmembrane protein 3), which holds promise for “stopping virus at the door,” says Nicholas Chesarino, a Ph.D. student at OSU and lead author of the study.
With climate change promising a wetter, warmer winter for 2015–16 in much of the U.S., the specter of flu season hovers on the edges of our daily lives, especially given that 2014’s vaccine was less effective than in recent years. When the correct flu strains are included, flu vaccines can be highly effective at preventing or lessening symptoms of flu. But the vaccine relies upon best guesses of flu strains and can’t always keep up with virus mutations.
Flu viruses break into healthy cells by what Chesarino calls a “two-step process.” First, the virus enters the body in a kind of “compartment.” Then it has to fuse its outer membrane to the cell membrane in order to take over the cell. If it doesn’t fuse, thanks to the body’s ability to fight it off, it gets destroyed by the body's defenses. This, he says, is where IFITM3 plays a crucial role.
“This protein prevents the virus from ever leaving the 'compartment,'” he tells mental_floss. “It basically stops the virus from establishing infection. That’s why our strategy is to increase levels of IFITM3 in cells. Because once the virus gets in, it can make thousands of copies of itself. But if we can prevent that one virus getting into the cell, we stop the infection in its tracks.”
Normally, IFITM3 is produced in large quantities only after the flu virus takes hold. Chesarino and his colleagues, led by Jacob Yount, senior author and assistant professor of microbial infection and immunity at OSU, discovered that inhibiting an enzyme called NEDD4, which is responsible for clearing out IFITM3 in the cells (a process known as ubiquitination), leaves behind high enough numbers of IFITM3 to prevent flu infection in mice and human lung cells. “This was a huge finding—that you don’t need an infection or interferon to increase the level of IFITM3.”
This new therapy is still in research and testing phases, but Chesarino says the results are encouraging: “This is a promising way to prevent flu at a universal level—something that wouldn’t have to change year to year. It also protects against new and emergent viruses such as avian and swine flu that transfer to humans.”
He is quick to point out that it won’t replace vaccines, but could be used in combination to overlap what vaccines lack in their functions. “A vaccine can’t protect against a virus humans haven’t seen before, whereas this therapy could make up for that,” he says.