This negative interaction may be driven by virus competition for susceptible cells, for example as a consequence of influenza-induced destruction of cell-surface receptors (35) and/or cell death (36), or as a consequence of virus-induced innate immune responses, such as the secretion of interferon (IFN), which can cause noninfected neighboring cells to adopt a protective antiviral state (23, 24). Here, IFNA1 is linked to influenza.