Studies On Infant Mice Offer A Novel Strategy To Stop The Flu From Spreading To Humans

It has long been known by scientists that many bacteria and viruses cause illnesses by first attaching themselves to sugar molecules on the cell surfaces lining mammals' sinuses and throats, including humans. For example, viral particles can cling to these molecules--also known as sialic acids, or SAs--in a manner similar to that of keys inserted into locks.

Now, a new study in infant mice shows that keeping virus particles from attaching to SAs limits more than just the entry of influenza A viral infections, but also hinders their exit (shedding) and transmission from mouse to mouse. Such infections are the main cause of the seasonal flu that kills more than 36,000 Americans annually. While vaccines to guard against infection and symptom treatments exist, they are not foolproof, scientists say, and more strategies are needed to prevent infection from spreading.

Led by researchers from NYU Grossman School of Medicine, the study team stripped away, or desialylated, SA receptors by placing directly into mouse nasal cavities a neuraminidase enzyme known to loosen the acids' ability to remain attached to cell surfaces. The infant mice were then infected with influenza A. Results showed treatment with the neuraminidase enzyme dramatically cut mouse-to-mouse transmission rates by more than half (from 51% to 100% ) in a half-dozen influenza strains tested.

Publishing in the American Society for Microbiology journal mBio online Jan.11, the work was conducted in infant mice, which unlike those even a few months older or adult mice, were found by the research team to have many sialic acids in the upper portion of their respiratory tract. Specifically, the team blocked two SAs, technically called alpha-2,3 SA and alpha-2,6 SA receptors (the locks). These...