Figure 3: Schematic diagram outlining the mechanisms of viral-bacterial synergistic interaction in bacterial co-infection during influenza pneumonia: Influenza viruses open neuraminidase site for the attachment of bacteria and predispose to bacterial co-infection. Bacterial infection amplifies viral proliferation by producing extracellular proteases for cleavage activation of influenza haemagglutinin. Influenza viruses with a potent innate immune response suppressing NS (e.g. as 1918PV, H5N1 and H7N9) produce a heavy viral load and induce cytokine dysregulation. This results in extensive pulmonary epithelial damage and predisposes to secondary bacterial infection.