Antiviral Defence Mechanisms during Early Mammalian Development
The type-I interferon (IFN) response constitutes the major innate immune pathway against viruses in mammals. Despite its critical importance for antiviral defence, this pathway is inactive during early embryonic development. There seems to be an incompatibility between the IFN response and pluripote...
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| Format: | Article |
| Language: | English |
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MDPI AG
2024-01-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/16/2/173 |
| _version_ | 1797296840501100544 |
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| author | Felix Mueller Jeroen Witteveldt Sara Macias |
| author_facet | Felix Mueller Jeroen Witteveldt Sara Macias |
| author_sort | Felix Mueller |
| collection | DOAJ |
| description | The type-I interferon (IFN) response constitutes the major innate immune pathway against viruses in mammals. Despite its critical importance for antiviral defence, this pathway is inactive during early embryonic development. There seems to be an incompatibility between the IFN response and pluripotency, the ability of embryonic cells to develop into any cell type of an adult organism. Instead, pluripotent cells employ alternative ways to defend against viruses that are typically associated with safeguard mechanisms against transposable elements. The absence of an inducible IFN response in pluripotent cells and the constitutive activation of the alternative antiviral pathways have led to the hypothesis that embryonic cells are highly resistant to viruses. However, some findings challenge this interpretation. We have performed a meta-analysis that suggests that the susceptibility of pluripotent cells to viruses is directly correlated with the presence of receptors or co-receptors for viral adhesion and entry. These results challenge the current view of pluripotent cells as intrinsically resistant to infections and raise the fundamental question of why these cells have sacrificed the major antiviral defence pathway if this renders them susceptible to viruses. |
| first_indexed | 2024-03-07T22:11:34Z |
| format | Article |
| id | doaj.art-ee334a36fc7f4750b3224e1461a2d60b |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-03-07T22:11:34Z |
| publishDate | 2024-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-ee334a36fc7f4750b3224e1461a2d60b2024-02-23T15:37:23ZengMDPI AGViruses1999-49152024-01-0116217310.3390/v16020173Antiviral Defence Mechanisms during Early Mammalian DevelopmentFelix Mueller0Jeroen Witteveldt1Sara Macias2Institute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, King’s Buildings, Charlotte Auerbach Road, Edinburgh EH9 3FL, UKInstitute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, King’s Buildings, Charlotte Auerbach Road, Edinburgh EH9 3FL, UKInstitute of Immunology and Infection Research, School of Biological Sciences, University of Edinburgh, King’s Buildings, Charlotte Auerbach Road, Edinburgh EH9 3FL, UKThe type-I interferon (IFN) response constitutes the major innate immune pathway against viruses in mammals. Despite its critical importance for antiviral defence, this pathway is inactive during early embryonic development. There seems to be an incompatibility between the IFN response and pluripotency, the ability of embryonic cells to develop into any cell type of an adult organism. Instead, pluripotent cells employ alternative ways to defend against viruses that are typically associated with safeguard mechanisms against transposable elements. The absence of an inducible IFN response in pluripotent cells and the constitutive activation of the alternative antiviral pathways have led to the hypothesis that embryonic cells are highly resistant to viruses. However, some findings challenge this interpretation. We have performed a meta-analysis that suggests that the susceptibility of pluripotent cells to viruses is directly correlated with the presence of receptors or co-receptors for viral adhesion and entry. These results challenge the current view of pluripotent cells as intrinsically resistant to infections and raise the fundamental question of why these cells have sacrificed the major antiviral defence pathway if this renders them susceptible to viruses.https://www.mdpi.com/1999-4915/16/2/173antiviralinterferoninnate immunityvirusdsRNAtransposable element |
| spellingShingle | Felix Mueller Jeroen Witteveldt Sara Macias Antiviral Defence Mechanisms during Early Mammalian Development Viruses antiviral interferon innate immunity virus dsRNA transposable element |
| title | Antiviral Defence Mechanisms during Early Mammalian Development |
| title_full | Antiviral Defence Mechanisms during Early Mammalian Development |
| title_fullStr | Antiviral Defence Mechanisms during Early Mammalian Development |
| title_full_unstemmed | Antiviral Defence Mechanisms during Early Mammalian Development |
| title_short | Antiviral Defence Mechanisms during Early Mammalian Development |
| title_sort | antiviral defence mechanisms during early mammalian development |
| topic | antiviral interferon innate immunity virus dsRNA transposable element |
| url | https://www.mdpi.com/1999-4915/16/2/173 |
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