Computation leads to better understanding of influenza virus replication

Computer simulations that reveal a key mechanism in the replication process of influenza A may help defend against future deadly pandemics. Treating influenza relies on drugs, such as Amantadine, that are becoming less effective due to viral evolution. But University of Chicago scientists have published computational results that may give drug designers the insight they need to develop the next generation of effective influenza treatment. "It's very hard to design a drug if you don't understand how the disease functions," said Gregory Voth, the Haig P. Papazian Distinguished Service Professor in Chemistry. Voth and three co-authors offer new insights into the disease's functioning in the Proceedings of the National Academy of Sciences Online Early Edition for the week of June 16-20. Amantadine is a bulky organic compound originally designed to treat influenza A by blocking proton flow through the M2 channel, one of the few proteins that are targets for antiviral therapies. "The proton flow is essential for influenza viral replication," said Voth, who also is director of the Center for Multiscale Theory and Simulation.