Matalon and colleagues showed that the flu virus damages our lungs through its "M2 protein," which attacks the cells that line the inner surfaces of our lungs (epithelial cells). Specifically, the M2 protein disrupts lung epithelial cells' ability to remove liquid from inside of our lungs, setting the stage for pneumonia and other lung problems. The researchers made this discovery by conducting three sets of experiments using the M2 protein and the lung protein they damage. First, frog eggs were injected with the lung protein alone to measure its function. Second, researchers injected frog eggs with both the M2 protein and the lung protein and found that the function of the lung protein was significantly decreased. Using molecular biology techniques, scientists isolated the segment of the M2 protein responsible for the damage to the lung protein. Then they demonstrated that without this segment, the protein was unable to cause damage. Third, the full M2 protein (with the "offending" segment intact) and the lung protein were then re-injected into the frog eggs along with drugs known to remove oxidants. This too prevented the M2 protein from causing damage to the lung protein. These experiments were repeated using cells from human lungs with exactly the same results.

"Although vaccines will remain the first line of intervention against the flu for a long time to come, this study opens the door for entirely new treatments geared toward stopping the virus after you're sick," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "and as Thanksgiving approaches, this discovery is another reason to drink red wine to your health."

Source: Federation of American Societies for Experimental Biology