With the except for the virus which spreads through the cell-cell fusion transmission, virus infection is initiated by the binding of cell-free virions to their host cells. Recently, the virus transmission mechanism from an infected cell to adjacent cells without virus diffusion into the extracellular environment is highlighted from the aspect of its significance in virus spreading in the presence of antibodies [1, 2] . This antibody-insensitive pathway is often called cell-to-cell transmission [2] . The cell-to-cell transmission may be categorized into two pathways, i.e., transmission of cell-free virions to adjacent uninfected cells, and transmission of progeny virions associated on the surface of an infected cell even after budding through narrow synaptic space between an infected cell and adjacent uninfected cells. As an example of the former mechanism, cell-free vaccinia virus particles associated with the filopodium of an infected cell are repelled toward neighboring uninfected cells by inducing the formation of actin filament [3] . Several cases have been reported for the latter mechanism: Immunotropic viruses including retroviruses utilize the immunological synapses [4] [5] [6] [7] . Immune cells are not constitutively polarized, but contain the machinery that directs their secretory apparatus towards a cell that is involved in an immunological synapse. This machinery can be subverted by retroviruses containing human immunodeficiency virus (HIV). An HIV-infected cell can polarize viral budding towards a target cell expressing receptor through a structure called a virological synapse. Virions bud from an infected cell into a synaptic cleft, from which they fuse with the target-cell plasma membrane [49] [50] [51] [52] . The progeny virions of HCV are trapped between infected and uninfected cell membranes at the tight junction. Using Claudin-1 known as a component of the tight junction and one of the entry factors of HCV [8] , virions fuse with and penetrate uninfected target cells [31] . Therefore, HCV may acquire the ability to spread within polarized liver epithelium. Thus, the cell-to-cell transmission certainly plays significant roles for the dissemination of several enveloped viruses. However, the cell-to-cell transmission of influenza virus has not been discussed well. Here, we have shown that influenza virus spreads by forming infected cell clusters even in the presence of an NA inhibitor. Live cell imaging clearly showed that influenza virus lacking the NA activity spreads from an infected cell to adjacent cells through the cell-to-cell transmission mechanism (Figure 2 ). This was also the case for wild-type influenza virus during early phases of infection ( Figure 4B ). In the cell-to-cell transmission of influenza virus, progeny virions could remain associated with the surface of infected cell even after budding, and then these progeny virions can be passed on to adjacent uninfected cells.