Lastly, more work is needed to ascertain the mechanistic role played by lung-resident and recruited granulocytes in SARS-CoV-2 control and pathogenesis (Camp and Jonsson, 2017, Flores-Torres et al., 2019). In contrast to their early protective role, neutrophil NETosis and macrophage crosstalk can drive later-stage inflammatory cascades (Barnes et al., 2020), underscoring the overall pathogenic nature of damage-sensing host responses (Figure 2).