Did researchers just take a big step toward a universal flu vaccine?


WITH more than a dozen different strains of influenza circulating the world at any given time, flu season is a bit like a box of chocolates: you never know what you’re going to get. That’s one reason why you need a flu shot every year. Different flu strains are constantly adapting different ways of evading your immune system’s defenses, and, so far, there is no single vaccine that can protect you from them all.
But scientists are making progress: A new vaccine candidate developed at the University of California, Los Angeles (UCLA), might bring researchers one step closer to universal flu protection. Engineered from multiple strains of the influenza virus, all of which have vulnerabilities to a specific type of protein in the immune system, the vaccine successfully protected test animals from two different strains of the flu in the lab.
The basis for the new vaccine candidate lies in a component of the immune system called interferons. When your immune system detects an infection, interferons are among the first responders on the scene, according to the study, published today (Jan. 18) in the journal Science. True to their name, the main function of these antiviral proteins is to interfere with the spread of viruses. They do this by signaling the danger to surrounding host cells, turning on multiple protective genes to promote a swift immune response that will, hopefully, kill the virus, and help the immune system adapt to the virus for long-lasting protection.
“If viruses do not induce interferons, they will not be killed in the first-line defense, and without interferons, the adaptive immune response is limited,” said seniorstudy author Ren Sun, a professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA, in a statement. “For these reasons, viruses have evolved strategies to evade detection and limit the production of interferons by host organisms.”
With this in mind, Sun and his colleagues spent four years researching the entire influenza genome in order to identify any mutations that either inhibit or enhance the host’s interferon response. Previous studies showed that it was possible to disable individual genetic sequences responsible for blocking interferons, but Sun and his colleagues were determined to go further, targeting multiple interferon-blocking sites to inhibit the virus as much as possible.
This research entailed sequencing every amino acid in the influenza genome, and ultimately allowed the researchers to identify eight mutations that made various influenza genes particularly sensitive to interferons.

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