The M2 proton channel from influenza A virus forms proton‐selective ion channels, which are the target of the drug amantadine. Here, existing experimental data are quantitatively examined for insights into mechanisms to account for the pH‐ and voltage‐dependences of M2 proton conduction. The analysis shows that a model involving protonation equilibria of His37, including pH‐dependent changes in the relative rates of diffusion on either side of the pore, is quantitatively able to account for recently reported electrophysiological data examining the pH‐ and voltage‐dependences of Rostock and Weybridge strain M2 proton conduction.