Measles virus (MV) is highly contagious virus that leads infant death worldwide. Humans are the unique natural reservoir for this virus. MV infection is characterized by virus-induced immune suppression that can lead to increased susceptibility to secondary bacterial and viral infections. The P, V and C proteins act as virulence factors to suppress innate immune response in host by inhibiting signaling for both type I IFN induction and JAK/STAT-mediated interferon-stimulated gene (ISG) induction. Moreover, H protein expressed on viral particles and binding to SLAM or CD46, as well as N protein liberated from infected cells and interacting with Fc-gamma R, causes an inhibition of IL-12 synthesis in dendritic cells. IL-12 is a key cytokine inducing cellular immune responses to protect host from the harm caused by pathogenic infections.