Indeed, in a mouse model of SARS-CoV-1, depletion of the C3 complement subunit attenuated SARS pathology (Gralinski et al., 2018), and anti-C5aR1 neutralizing antibodies inhibited the C5a-mediated recruitment of human myeloid cells to lung tissue and reduced accompanying lung injury in a humanized mouse model (Carvelli et al., 2020). This evidence concerns the gene C3 and severe acute respiratory syndrome.