Phagocytosis of influenza virus-infected cells undergoing apoptosis by macrophages is well recognized as a protective host response against the virus infection. Cultured chorion cells secrete a factor with monocyte differentiation-inducing (MDI) activity (MDI factor) during apoptotic cellular degradation after influenza virus infection.  Pro-inflammatory cytokines, such as interleukin (IL)-6, tumor necrosis factor (TNF)-α and interferon (IFN)-β, are identified as a member of the MDI factor. The MDI factor induces the mRNA expression of macrophage class A scavenger receptor, one of adhesion and apoptotic cell-recognizing molecules, and gp91^phox, a catalytic subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme complex, resulting in the differentiation of monocytes to well-matured macrophages that are capable of adhering, phagocytosing and producing superoxide through NADPH oxidase. The matured macrophages treated with the MDI factor are able to phagocytose apoptotic chorion cells resulting from the virus infection. Therefore, the MDI factor, which is composed of IL-6, TNF-α and IFN-β, plays a critical role in the facilitating phagocytosis of apoptotic cells by matured macrophages during influenza virus infection.  This article summarizes a recent knowledge regarding a hypothetical mechanism of apoptosis induction by influenza virus infection in cultured chorion cells, and the molecular and biological characteristics of the MDI factor derived from the virus-infected cells.