Last spring, with fears rising over the H1N1 swine flu virus, researchers from the University of Illinois at Urbana-Champaign and the University of Utah were granted emergency supercomputing time at the Texas Advanced Computing Center in Austin. Their goal: to model the virus's possible resistance to medications such as Tamiflu (white molecule, center of image). These antiviral drugs bind to a surface protein, called neuraminidase, that influenza uses to infect host cells.
Two weeks of continuous calculations on the supercomputer showed that the neuraminidase-binding site has a mostly negative charge (red); it is surrounded by positively charged regions (purple), with a narrow negative-charge pathway for the drug to follow. Mutations to proteins along that delivery route could make the H1N1 virus resistant to drugs, although for now it remains vulnerable.