Our study is in agreement with this finding, showing that NOX2 dependent ROS production to virus infection and to the TLR7 agonist imiquimod was abolished in TLR7−/− cells and also by pretreatment with bafilomycin A. Second, bafilomycin A suppressed PKC activation due to influenza virus and imiquimod treatment, and PKC is upstream of acute NOX2 activation10, 11. This evidence concerns the gene TLR7 and viral infectious disease.