Researchers at the University of California, San Diego (UCSD) School of Medicine have shown, for the first time, how influenza A viruses snip through a protective mucus net to both infect respiratory cells and later cut their way out to infect other cells. The findings, published online in an open-access article in the Virology Journal by principal investigator Pascal Gagneux, Ph.D., associate professor in the Department of Cellular and Molecular Medicine, and colleagues, could point the way to new drugs or therapies that more effectively inhibit viral activity, and perhaps prevent some flu infections altogether. Scientists have long known that common strains of influenza specifically seek out and exploit sialic acids, a class of signaling sugar molecules that cover the surfaces of all animal cells. The ubiquitous H1N1 and H3N2 flu strains, for example, use the protein hemagglutinin (H) to bind to matching sialic acid receptors on the surface of a cell before penetrating it, and then use the enzyme neuraminidase (N) to cleave or split these sialic acids when viral particles are ready to exit and spread the infection. Mucous membrane cells, such as those that line the internal airways of the lungs, nose, and throat, defend themselves against such pathogens by secreting a mucus rich in sialic acids – a gooey trap intended to bog down viral particles before they can infect vulnerable cells. "The sialic acids in the secreted mucus act like a sticky spider's web, drawing viruses in and holding them by their hemagglutinin proteins," said Dr. Gagneux. Using a novel technique that presented viral particles with magnetic beads coated with different forms of mucin (the glycoproteins that comprise mucus) and varying known amounts of sialic acids, Dr.
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