Bone marrow stromal Ag 2 (BST2) is a transmembrane protein that prevents virus release from infected cells. It was also reported that BST2 inhibits type I IFN production by plasmacytoid dendritic cells. To determine BST2 impact on antiviral responses in vivo, we generated BST2 -/- mice. Following infection with a murine retrovirus, BST2 -/- mice had slightly elevated viral loads; however, infection with other enveloped viruses revealed unexpected roles of BST2. BST2 -/- mice showed reduced type I IFN production by plasmacytoid dendritic cells. Moreover, BST2 -/- mice had lower viral titers in lungs following intranasal infection with vesicular stomatitis virus expressing OVA and influenza B and increased numbers of virus-specific CD8 T cells in the lungs, suggesting that BST2 may facilitate entry and/or replication of enveloped viruses and modulate priming of CD8 T cells. These findings suggest complex roles of BST2 beyond retroviral control in vivo, possibly reflecting the involvement of BST2 in endocytosis and intracellular trafficking of viruses, viral nucleic acids, and Ags.

Original languageEnglish
Pages (from-to)2488-2492
Number of pages5
JournalJournal of Immunology
Issue number6
StatePublished - Mar 15 2012


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