In an experimental mouse model of MERS-CoV, increased concentrations of the C5a and C5b-9 complement products were found in sera and lungs, respectively, and inhibition of complement activation with anti-C5a reduced lung damage (41, 64, 66). In another experimental mouse model of SARS-CoV infection, C3 invalidation was associated with substantial reductions in tissue lesions and recruitment of inflammatory cells in the lungs, suggesting that the complement may play a significant role in the early step of inflammation (67). The gene discussed is C5AR1; the disease is severe acute respiratory syndrome.