| First Author | Londrigan SL | Year | 2015 |
| Journal | PLoS One | Volume | 10 |
| Issue | 11 | Pages | e0142925 |
| PubMed ID | 26566124 | Mgi Jnum | J:244727 |
| Mgi Id | MGI:5913506 | Doi | 10.1371/journal.pone.0142925 |
| Citation | Londrigan SL, et al. (2015) Endogenous Murine BST-2/Tetherin Is Not a Major Restriction Factor of Influenza A Virus Infection. PLoS One 10(11):e0142925 |
| abstractText | BST-2 (tetherin, CD317, HM1.24) restricts virus growth by tethering enveloped viruses to the cell surface. The role of BST-2 during influenza A virus infection (IAV) is controversial. Here, we assessed the capacity of endogenous BST-2 to restrict IAV in primary murine cells. IAV infection increased BST-2 surface expression by primary macrophages, but not alveolar epithelial cells (AEC). BST-2-deficient AEC and macrophages displayed no difference in susceptibility to IAV infection relative to wild type cells. Furthermore, BST-2 played little role in infectious IAV release from either AEC or macrophages. To examine BST-2 during IAV infection in vivo, we infected BST-2-deficient mice. No difference in weight loss or in viral loads in the lungs and/or nasal tissues were detected between BST-2-deficient and wild type animals. This study rules out a major role for endogenous BST-2 in modulating IAV in the mouse model of infection. |
