Abstract
BST2/tetherin is a transmembrane protein with antiviral activity; it is synthesized following exposure to interferons, and restricts the release of budding virus particles by tethering them to the host cell membrane. We previously showed that BST2 is induced in primary neurons following measles virus (MV) infection or type I interferon; however, BST2 was dispensable for protection against challenge with neuron-restricted MV. Here, we define the contribution of BST-2 in neuronal MV infection. Surprisingly, and in contrast to its antiviral role in non-neuronal cells, murine BST2 promotes MV infection in brains of permissive mice and in primary neuron cultures. Moreover, BST2 expression was predominantly observed in the non-synaptic fraction of purified neurons. These studies highlight a cell-type dependent role of a well-characterized antiviral protein in enhancing neuronal infection.