Researchers have discovered that it may be possible to stop the flu by manipulating a certain protein in the body, preventing the disease without vaccines.

The flu vaccine is the primary method by which the flu is prevented. However, it is not 100 percent effective because the flu vaccine is developed based on a projection of which virus strain will be taking center stage during the coming flu season. Strains mutate every year so this means that it's entirely possible that a flu vaccine will be useless against the prevailing strain.

What Jacob Yount and colleagues are working on is to prevent the disease from even developing in the first place, not fight it. After seeing that altering the function of one protein can halt the virus, the researchers began experimenting on mice to further explore the discovery, resulting in a study published in the journal PLOS Pathogens.

The interferon-induced transmembrane protein 3, or IFITM3, is a protein effective against all strains of the flu ever recorded. The trick to making the most out of it then is to boost levels of the protein in cells before the body is exposed to the flu virus. Under normal conditions, the body produces large quantities of IFITM3 when a flu virus is detected to reduce the severity of an infection. But when a virus doesn't show, IFITM3 is degraded.

When cells spot the flu virus, they crank up interferon production, which also boosts IFITM3 levels. Interferon has another purpose though: signaling an enzyme called NEDD4 to stop degrading IFITM3 so the protein can work to fight the virus.

The researchers focused on NEDD4 and were able to show that inhibiting the enzyme led to IFITM3 accumulation, which offered greater resistance against infections from flu viruses. They opted out of stimulating interferon production to boost IFITM3 levels because high interferon levels leads to side effects, which includes flu-like symptoms.

Interferon is still needed to jump-start the production of IFTM3 but the researchers only induced one response. That was enough to put IFITM3 in a steady-state level if NEDD4 will be removed anyway.

The researchers are still working on how and when to get rid of the enzyme because experiments with mice showed NEDD4 was crucial for embryos to survive birth, indicating an importance associated with fetal development. Getting rid of NEDD4 later in life doesn't pose health problems for adult mice though, which is what Young and his colleagues are using now as subjects.

The study received funding support from the National Institute for Allergy and Infectious Diseases. Other authors include Nicholas Chesarino and Temet McMichael.

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