Human retroviruses such as HIV-1 and HTLV-1 spread more efficiently between target T cells by cell-cell infection than by cell-free infection [159, 160] . Sattentau et al. proposed, in analogy to the "immunological synapse", the "virological synapse (VS)" as a point of contact between virusinfected cells and uninfected cells [161, 162] . The molecular mechanisms of retroviral VS formation are as follows. (1) With respect to HIV-1 T-cell VS, initial contact between virus-infected cells and uninfected cells occurs through gp120-CD4 binding. Subsequent interactions between integrins and ICAMs enforce and maintain the stability of these junctions. (2) The gp120-CD4 interaction recruits CD4, coreceptors such as CXCR or CCR5, adhesion molecules, and filamentous actin into the synaptic area. (3) The cellular secretory machinery and microtubule organizing centers (MTOC) are polarized towards the HIV-1 assembly sites at the PM to form the VS. It has been reported that a socalled microsynapse formed by nanotubes between virusinfected cells and uninfected cells is also involved in cell-cell infection of HIV-1 [84, 163] . In cell-cell transfer of HTLV-1-infected cells, an extracellular matrix structure referred to as the "viral biofilm" was proposed as an alternative to the VS [164] . In addition to HIV-1 and HTLV-1, the spread of MLV between fibroblasts also occurs via the VS [165, 166] . It is noteworthy that assembly of MLV is directed towards cellcell contact sites through the interaction of the CT of MLV Env with Gag [167, 168] . Although the concept of cell-cell infection through the VS is now well appreciated, the detailed molecular mechanism of VS assembly and its relevance to viral spread in vivo will require further elucidation through the use of more advanced techniques.