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The role of BST‐2/Tetherin in host protection and disease manifestation
Host cells respond to viral infections by activating immune response genes that are not only involved in inflammation, but may also predispose cells to cancerous transformation. One such gene is BST‐2, a type II transmembrane protein with a unique topology that endows it tethering and signaling pote...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768070/ https://www.ncbi.nlm.nih.gov/pubmed/27042298 http://dx.doi.org/10.1002/iid3.92 |
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author | Mahauad‐Fernandez, Wadie D. Okeoma, Chioma M. |
author_facet | Mahauad‐Fernandez, Wadie D. Okeoma, Chioma M. |
author_sort | Mahauad‐Fernandez, Wadie D. |
collection | PubMed |
description | Host cells respond to viral infections by activating immune response genes that are not only involved in inflammation, but may also predispose cells to cancerous transformation. One such gene is BST‐2, a type II transmembrane protein with a unique topology that endows it tethering and signaling potential. Through this ability to tether and signal, BST‐2 regulates host response to viral infection either by inhibiting release of nascent viral particles or in some models inhibiting viral dissemination. However, despite its antiviral functions, BST‐2 is involved in disease manifestation, a function linked to the ability of BST‐2 to promote cell‐to‐cell interaction. Therefore, modulating BST‐2 expression and/or activity has the potential to influence course of disease. |
format | Online Article Text |
id | pubmed-4768070 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-47680702016-04-01 The role of BST‐2/Tetherin in host protection and disease manifestation Mahauad‐Fernandez, Wadie D. Okeoma, Chioma M. Immun Inflamm Dis Review Host cells respond to viral infections by activating immune response genes that are not only involved in inflammation, but may also predispose cells to cancerous transformation. One such gene is BST‐2, a type II transmembrane protein with a unique topology that endows it tethering and signaling potential. Through this ability to tether and signal, BST‐2 regulates host response to viral infection either by inhibiting release of nascent viral particles or in some models inhibiting viral dissemination. However, despite its antiviral functions, BST‐2 is involved in disease manifestation, a function linked to the ability of BST‐2 to promote cell‐to‐cell interaction. Therefore, modulating BST‐2 expression and/or activity has the potential to influence course of disease. John Wiley and Sons Inc. 2015-12-07 /pmc/articles/PMC4768070/ /pubmed/27042298 http://dx.doi.org/10.1002/iid3.92 Text en © 2015 The Authors. Immunity, Inflammation and Disease Published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Mahauad‐Fernandez, Wadie D. Okeoma, Chioma M. The role of BST‐2/Tetherin in host protection and disease manifestation |
title | The role of BST‐2/Tetherin in host protection and disease manifestation |
title_full | The role of BST‐2/Tetherin in host protection and disease manifestation |
title_fullStr | The role of BST‐2/Tetherin in host protection and disease manifestation |
title_full_unstemmed | The role of BST‐2/Tetherin in host protection and disease manifestation |
title_short | The role of BST‐2/Tetherin in host protection and disease manifestation |
title_sort | role of bst‐2/tetherin in host protection and disease manifestation |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768070/ https://www.ncbi.nlm.nih.gov/pubmed/27042298 http://dx.doi.org/10.1002/iid3.92 |
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