Mechanism of Rhinovirus Immunity and Asthma
The majority of asthma exacerbations in children are caused by Rhinovirus (RV), a positive sense single stranded RNA virus of the Picornavirus family. The host has developed virus defense mechanisms that are mediated by the upregulation of interferon-activated signaling. However, the virus evades th...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2021-10-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2021.731846/full |
| _version_ | 1818406315115937792 |
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| author | Zuqin Yang Hannah Mitländer Tytti Vuorinen Susetta Finotto |
| author_facet | Zuqin Yang Hannah Mitländer Tytti Vuorinen Susetta Finotto |
| author_sort | Zuqin Yang |
| collection | DOAJ |
| description | The majority of asthma exacerbations in children are caused by Rhinovirus (RV), a positive sense single stranded RNA virus of the Picornavirus family. The host has developed virus defense mechanisms that are mediated by the upregulation of interferon-activated signaling. However, the virus evades the immune system by inducing immunosuppressive cytokines and surface molecules like programmed cell death protein 1 (PD-1) and its ligand (PD-L1) on immunocompetent cells. Initially, RV infects epithelial cells, which constitute a physiologic mucosal barrier. Upon virus entrance, the host cell immediately recognizes viral components like dsRNA, ssRNA, viral glycoproteins or CpG-DNA by host pattern recognition receptors (PRRs). Activation of toll like receptors (TLR) 3, 7 and 8 within the endosome and through MDA-5 and RIG-I in the cytosol leads to the production of interferon (IFN) type I and other antiviral agents. Every cell type expresses IFNAR1/IFNAR2 receptors thus allowing a generalized antiviral activity of IFN type I resulting in the inhibition of viral replication in infected cells and preventing viral spread to non-infected cells. Among immune evasion mechanisms of the virus, there is downregulation of IFN type I and its receptor as well as induction of the immunosuppressive cytokine TGF-β. TGF-β promotes viral replication and is associated with induction of the immunosuppression signature markers LAP3, IDO and PD-L1. This article reviews the recent advances on the regulation of interferon type I expression in association with RV infection in asthmatics and the immunosuppression induced by the virus. |
| first_indexed | 2024-12-14T09:09:59Z |
| format | Article |
| id | doaj.art-c875f7c7393c470a93ae2cd6b5273862 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-14T09:09:59Z |
| publishDate | 2021-10-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-c875f7c7393c470a93ae2cd6b52738622022-12-21T23:08:35ZengFrontiers Media S.A.Frontiers in Immunology1664-32242021-10-011210.3389/fimmu.2021.731846731846Mechanism of Rhinovirus Immunity and AsthmaZuqin Yang0Hannah Mitländer1Tytti Vuorinen2Susetta Finotto3Department of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, GermanyDepartment of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, GermanyMedical Microbiology, Turku University Hospital, Institut of Biomedicine, University of Turku, Turku, FinlandDepartment of Molecular Pneumology, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, GermanyThe majority of asthma exacerbations in children are caused by Rhinovirus (RV), a positive sense single stranded RNA virus of the Picornavirus family. The host has developed virus defense mechanisms that are mediated by the upregulation of interferon-activated signaling. However, the virus evades the immune system by inducing immunosuppressive cytokines and surface molecules like programmed cell death protein 1 (PD-1) and its ligand (PD-L1) on immunocompetent cells. Initially, RV infects epithelial cells, which constitute a physiologic mucosal barrier. Upon virus entrance, the host cell immediately recognizes viral components like dsRNA, ssRNA, viral glycoproteins or CpG-DNA by host pattern recognition receptors (PRRs). Activation of toll like receptors (TLR) 3, 7 and 8 within the endosome and through MDA-5 and RIG-I in the cytosol leads to the production of interferon (IFN) type I and other antiviral agents. Every cell type expresses IFNAR1/IFNAR2 receptors thus allowing a generalized antiviral activity of IFN type I resulting in the inhibition of viral replication in infected cells and preventing viral spread to non-infected cells. Among immune evasion mechanisms of the virus, there is downregulation of IFN type I and its receptor as well as induction of the immunosuppressive cytokine TGF-β. TGF-β promotes viral replication and is associated with induction of the immunosuppression signature markers LAP3, IDO and PD-L1. This article reviews the recent advances on the regulation of interferon type I expression in association with RV infection in asthmatics and the immunosuppression induced by the virus.https://www.frontiersin.org/articles/10.3389/fimmu.2021.731846/fullasthmarhinovirushost defenseimmune evasioninterferon type I |
| spellingShingle | Zuqin Yang Hannah Mitländer Tytti Vuorinen Susetta Finotto Mechanism of Rhinovirus Immunity and Asthma Frontiers in Immunology asthma rhinovirus host defense immune evasion interferon type I |
| title | Mechanism of Rhinovirus Immunity and Asthma |
| title_full | Mechanism of Rhinovirus Immunity and Asthma |
| title_fullStr | Mechanism of Rhinovirus Immunity and Asthma |
| title_full_unstemmed | Mechanism of Rhinovirus Immunity and Asthma |
| title_short | Mechanism of Rhinovirus Immunity and Asthma |
| title_sort | mechanism of rhinovirus immunity and asthma |
| topic | asthma rhinovirus host defense immune evasion interferon type I |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2021.731846/full |
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