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| Content Provider | PubMed Central |
|---|---|
| Author | Chesnokova, Liudmila S. Nishimura, Stephen L. Hutt-fletcher, Lindsey M. |
| Abstract | Epstein–Barr, virus (EBV) is a ubiquitous human herpesvirus that is causally implicated in the development of lymphoid and epithelial tumors. Entry of virus requires fusion of virus envelopes and cell membranes. Fusion with B lymphocytes requires virus glycoprotein gB and a 3-part complex of glycoproteins, gHgLgp42. It is triggered by interactions between glycoprotein 42 (gp42) and HLA class II. However, fusion with epithelial cells is impeded by gp42 and instead is triggered by interactions between an unknown epithelial protein and a 2-part complex of gHgL. We report here that gHgL binds with high affinity to epithelial cells and that affinity of binding is increased by 3 orders of magnitude in the presence of Mn2+. Binding and infection can be reduced by fibronectin and vitronectin, by down-regulation of integrin αv, or by a peptide corresponding to 13 aa of gH which include a KGDE motif. Fusion of cells expressing gB and gHgL can be blocked by vitronectin or triggered by addition of soluble truncated integrins αvβ6 and αvβ8. We conclude that the direct interaction between EBV gHgL and integrins αvβ6 and αvβ8 can provide the trigger for fusion of EBV with an epithelial cell. |
| Related Links | http://dx.doi.org/10.1073/pnas.0907508106 |
| Starting Page | 20464 |
| File Format | |
| ISSN | 10916490 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 48 |
| Volume Number | 106 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2009-12-01 |
| Access Restriction | Open |
| Rights Holder | National Academy of Sciences |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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