Commit b3f36a1b authored by Marek Ostaszewski's avatar Marek Ostaszewski
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Merge branch 'patch-1' into 'master'

Update PAMP Readme

See merge request !240
parents 3776710b 240810cd
...@@ -9,6 +9,19 @@ Viral proteins that interfere with these pathways are included in the map. Sars- ...@@ -9,6 +9,19 @@ Viral proteins that interfere with these pathways are included in the map. Sars-
The map contains the initial recognition process of the viral particle by the innate immune system and the viral mechanisms to evade the immune response. It provides the connection between the virus entry (detecting the endosomal viral patterns), the virus replication cycle (detection cytoplasmatic viral patterns), and the effector pathways of pro-inflammatory cytokines, especially of the interferon type I class. Latter seems to play a crucial but complex role in the Covid-19 pathology. In vitro and in vivo (the latter only for Sars-Cov-1, yet) administration of Interferons (as antiviral cytokines in the immune defense) has resulted in a dose-dependent reduction of the virus titer [8], [9]. Contradictory, multiple studies have shown that ACE2, one of the main entry proteins for Sars-Cov-2 belongs to the interferon-stimulated genes (ISGs), providing arguments for a positive effect of interferons on the virus replication [10], [11]. The molecular pathways behind the Covid-19 pathology are complex and are probably the result of very specific regulatory mechanisms causing the virus’ infectiousness. Clarifying the mechanisms of how Sars-Cov-2 modulates the innate immune defense in its favor to either evade recognition or, on the other hand, stimulate the immune response to amplify its replication is crucial to understand the virus pathology. The map contains the initial recognition process of the viral particle by the innate immune system and the viral mechanisms to evade the immune response. It provides the connection between the virus entry (detecting the endosomal viral patterns), the virus replication cycle (detection cytoplasmatic viral patterns), and the effector pathways of pro-inflammatory cytokines, especially of the interferon type I class. Latter seems to play a crucial but complex role in the Covid-19 pathology. In vitro and in vivo (the latter only for Sars-Cov-1, yet) administration of Interferons (as antiviral cytokines in the immune defense) has resulted in a dose-dependent reduction of the virus titer [8], [9]. Contradictory, multiple studies have shown that ACE2, one of the main entry proteins for Sars-Cov-2 belongs to the interferon-stimulated genes (ISGs), providing arguments for a positive effect of interferons on the virus replication [10], [11]. The molecular pathways behind the Covid-19 pathology are complex and are probably the result of very specific regulatory mechanisms causing the virus’ infectiousness. Clarifying the mechanisms of how Sars-Cov-2 modulates the innate immune defense in its favor to either evade recognition or, on the other hand, stimulate the immune response to amplify its replication is crucial to understand the virus pathology.
## References
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- [5] K. L. Siu, K. H. Kok, M. H. J. Ng, et al., “Severe acute respiratory syndrome coronavirus M protein inhibits type I interferon production by impeding theformation of TRAF3·TANK·TBK1/IKKε complex,” J. Biol. Chem., vol. 284, no. 24, pp. 16202–16209, Jun. 2009, doi: 10.1074/jbc.M109.008227.
- [6] X. Fang, J. Gao, H. Zheng, et al., “The membrane protein of SARS-CoV suppresses NF-κB activation,” J. Med. Virol., vol. 79, no. 10, pp. 1431–1439, Oct. 2007, doi: 10.1002/jmv.20953.
- [7] Q. J. Liao, L. B. Ye, K. A. Timani, et al., “Activation of NF-κB by the full-length nucleocapsid protein of the SARS coronavirus,” Acta Biochim. Biophys. Sin. (Shanghai)., vol. 37, no. 9, pp. 607–612, Sep. 2005, doi: 10.1111/j.1745-7270.2005.00082.x.
- [8] E. Mantlo, N. Bukreyeva, J. Maruyama, et al., “Antiviral activities of type I interferons to SARS-CoV-2 infection,” Antiviral Res., vol. 179, p. 104811, Jul. 2020, doi: 10.1016/j.antiviral.2020.104811.
- [9] T. Kuri, X. Zhang, M. Habjan, et al., “Interferon priming enables cells to partially overturn the SARS coronavirus-induced block in innate immune activation,” J. Gen. Virol., vol. 90, no. 11, pp. 2686–2694, 2009, doi: 10.1099/vir.0.013599-0.
- [10] C. G. K. Ziegler, S. J. Allon, S. K. Nyquist, et al., “SARS-CoV-2 Receptor ACE2 Is an Interferon-Stimulated Gene in Human Airway Epithelial Cells and Is Detected in Specific Cell Subsets across Tissues,” Cell, vol. 181, no. 5, pp. 1016-1035.e19, May 2020, doi: 10.1016/j.cell.2020.04.035.
- [11] S. Su and S. Jiang, “A suspicious role of interferon in the pathogenesis of SARS-CoV-2 by enhancing expression of ACE2,” Signal Transduct. Target. Ther., vol. 5, no. 1, p. 71, May 2020, doi: 10.1038/s41392-020-0185-z.
## Creators ## Creators
- [Matti Hoch](https://fairdomhub.org/people/1520) - [Matti Hoch](https://fairdomhub.org/people/1520)
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