Shedding new light on how influenza virus attacks the lungs, a new study conducted by researchers has provided targets for new treatments.
Writing about their findings in the online edition of the Federation of American Societies for Experimental Biology, the researchers at the University of Alabama at Birmingham (UAB) and Southern Research Institute have revealed that a protein in influenza virus called M2, which helps it multiply, also damages lung epithelial cells, causing fluid build-up in the lungs.
They say that the accumulation of fluid in the lungs makes it difficult for the patient to breathe and prevents oxygen from reaching the blood stream.
Oxidants are necessary for proper cell function, they point out, but can become toxic if uncontrolled.
"Under normal conditions, oxidants play an important role, as they destroy pathogens in cells. But our findings suggest that lowering the number of oxidants, or preventing their increase, would prevent damage to the lungs resulting from the M2 protein," said principal investigator Dr. Sadis Matalon, vice chairman for research and professor of anesthesiology at UAB.
During the study, the researchers injected frog eggs with M2 protein and the lung protein involved with fluid removal.
They used molecular biology techniques to remove part of the flu protein until they could isolate the segment responsible for the lung injury.
"We found that when the flu protein was shortened in length, it did not damage the lung protein responsible for removing fluid from the lungs. This is important information as it will enable us to design drugs that will hopefully prevent this M2 flu protein from functioning properly, making it possible for those infected with the flu to recover faster," said Dr. Diana L. Noah, of Southern Research.
In another set of experiments, the researchers injected intact flu proteins and their target lung proteins into frog eggs, along with agents that remove oxidants.
According to them, following this procedure the lung proteins were no longer damaged by the flu viruses.
When the researchers repeated the experiments in cells from human lungs, they found the same results.
"We were able to understand the basic mechanisms by which the flu damages key components of the lungs in a simple system, such as the frog eggs, and then confirm these findings in human lung cells," said Matalon.
The researches, however, have not said as yet whether their results could be understood to mean that a simple antioxidant, such as vitamin C, can prevent or minimize flu.
"The issue is too complex and we simply can't answer that yet. Vaccination is our leading defense against flu and we have anti-viral drugs that are effective in some cases, but flu viruses show a remarkable ability to mutate, rendering vaccines and drugs less effective. Having a new target for potential interventions opens up an entirely new approach to combating influenza," said James W. Noah, of Southern Research.
Funding for the study came from the National Heart, Blood and Lung Institute, and the National Institute of Environmental Health Sciences, parts of the National Institutes of Health, and the UAB Department of Anesthesiology.