An anti-virus drug attacks influenza A by changing the motion and structure of a proton channel necessary for the virus to infect healthy cells, according to a recently published research paper by two Iowa State University chemists.
Mei Hong, Iowa State's John D. Corbett Professor in Chemistry, and Sarah Cady, a graduate student in chemistry, are studying the effects of the antiviral drug amantadine on influenza A. That's the type of flu bug that most commonly makes people sick and the one that has caused the most serious flu epidemics.
Their findings appear in the Feb. 5 edition of the Proceedings of the National Academy of Sciences.
Hong said the findings are particularly important because mutations of the type A virus are resistant to amantadine treatment.
“In the last few years, amantadine resistance has skyrocketed among influenza A viruses in Asia and North America, making it imperative to develop alternative antiviral drugs,” Hong and Cady wrote in their paper.
To develop those drugs, Hong said researchers first need to understand exactly how amantadine stops the flu virus.
First, some background about how a flu virus infects a healthy cell: A virus begins the process by attaching itself to a healthy cell. The healthy cell surrounds the flu virus and takes it inside the cell through a process called endocytosis. Once in the cell, the virus uses a protein called M2 to open a channel to the healthy cell. Protons from the healthy cell flow through the channel into the virus and raise its acidity. That triggers the release of the virus' genetic material into the healthy cell. The virus hijacks the healthy cell's resources and uses them to reproduce and spread the virus.
If the M2 proton channel is blocked, the process doesn't work and a virus can't infect a cell and spread.