Mothes's group had already shown that viruses surf along the outer surface of filopodia toward the cell body. Now they find that infected fibroblasts deposit retroviral particles onto their neighbors' filopodia.
Infected cells grab filopodia using contacts between a transmembrane retroviral protein and its receptor in the uninfected cell. At the meeting point, the already infected cell tears off and takes in chunks of filopodial membrane by endocytosis. “The infected cell pulls the target cell into itself,” explains Mothes. “The forces must be gigantic.” These forces lengthen and stabilize the structure into a bridge that resembles cytonemes, the actin-filled communication tubes that connect fly epithelial cells.
Retroviral particles assembled at the endocytic hot spots, which abutted the filopodial tips. The particles then budded out onto the filopodia. A mutant version of the viral budding protein blocked their escape. By linking to the filopodial actin network, the particles then moved against the membrane tide toward the uninfected cell, where they were eventually internalized.