Application of RXR in construction of susceptibility model of herpes simplex virus type 1 (HSV-1)

A technology of herpes simplex virus, HSV-1, applied in the field of biomedicine

Inactive Publication Date: 2016-06-15
宁波美丽人生医药生物科技发展有限公司
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

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Problems solved by technology

; For example, specific inhibitors of cyclooxygenase 1 increase the replication of pseudorabies virus PFV (Ray et al. 2004). Mice given cyclooxygenase 1 knockout but not given cyclooxygenase 2 knockout are more resistant to influenza virus Invasion (Carey et al. 2005) and cyclooxygenase 1 promoter hyperacetylation produces interferon repression in histone deacetylation-deficient macrophages (Chen et al. 2012) Although multiple studies have shown that cyclooxygenase 1 regulates Inhibition of type 1 interferons, but regulation of cyclooxygenase 1 by host antiviral responses remains poorly studied

Method used

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  • Application of RXR in construction of susceptibility model of herpes simplex virus type 1 (HSV-1)
  • Application of RXR in construction of susceptibility model of herpes simplex virus type 1 (HSV-1)
  • Application of RXR in construction of susceptibility model of herpes simplex virus type 1 (HSV-1)

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Experimental program
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Effect test

Embodiment 1

[0048] RXR expression regulates host susceptibility to herpes simplex virus type 1 (HSV-1) infection:

[0049] Our previous genetic studies have established a novel interferon regulator 3-dependent but interferon-independent mechanism to downregulate RXR expression (Chow et al. 2006). To determine RXR expression levels by different types of virus infection, bone marrow-derived macrophages were infected with herpes simplex virus type 1. The results showed that the expression of RXR was down-regulated after infection with the above viruses (such as figure 1 shown in A). Repression of the RXR gene was not due to changes in the cell state after infection, as the L32 control gene was unchanged (data not shown). Administration of the RNA virus analogue polyI:C and the DNA virus analogue polydA:dT can activate intracellular virus and also significantly inhibit the expression of RXR in bone marrow macrophages. (Such as figure 1 Shown in B) More importantly, it confirms that this s...

Embodiment 2

[0053] Ligand activation of RXR inhibits the expression of multiple antiviral genes:

[0054] In order to study how RXR weakens the host immune response and facilitates virus infection, the inventors of the present invention performed gene chip detection on the RXR agonist pretreatment group and macrophage PolyI:C transfection group. The results show that 9 cis retinoic acid can inhibit a variety of Poly1:C-induced genes, including type 1 interferon genes (such as IFN1, IFN2, IFN4, IFN5) Isg15, Ifit3 and Gbp3 (such as image 3 A) Considering that type 1 interferon and its downstream interferon-stimulated gene ISGs play an important role in the host's immune response in antiviral infection, RXR-mediated inhibition of these antiviral genes may be the host's response to viral infection caused by susceptibility. In order to verify the genetic data and prove the hypothesis that RXR is beneficial to virus infection by inhibiting antiviral genes, the inventors pretreated RAW264.7 ce...

Embodiment 4

[0056] RXR inhibits the transcription of interferon by targeting and regulating the downstream RIG-1 and TLR3 signaling pathways:

[0057] In order to further study how RXR inhibits type 1 interferon, the present inventors applied the interferon catalyst luciferase receptor (IFN-luc) and found that the 9-cis retinoic acid-treated group transfected by PolyI:C significantly reduced the interference Activation of the prime promoter. (Such as Figure 4 shown in A). These data suggest that RXR represses interferon transcription.

[0058] The transfected PolyI:C can be recognized by TLR3 and RIG-1, and TLR3 and RIG-1 recruit downstream adapter molecules IPS1 and TRIF, respectively. Both IPS1 and TRIF can promote the phosphorylation of TBK1 kinase and interferon regulatory factor 3, and then the dimer of interferon regulatory factor 3 enters the nucleus to promote interferon transcription (Newton and Dixit2012; Takeuchi and Akira2009, 2010). Co-overexpression of RXR significantly...

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Abstract

The invention especially relates to application of RXR in construction of a susceptibility model of HSV-1, which belongs to the field of biological medicine. The invention provides application of RXR in construction of the susceptibility model of HSV-1 and a construction method for a susceptible cell model of HSV-1 caused by overexpression of RXR. It is found that a COX susception pathway plays a critical role in host defense against HSV-1 in an RXR dependence manner. Application of RXR in construction of the susceptibility model of HSV-1 is further expounded.

Description

Technical field: [0001] The invention relates to the field of biomedicine, in particular to the use of RXR in constructing a type 1 herpes simplex virus (HSV-1) susceptibility model. Background technique [0002] Immune activation during viral infection leads to downregulation of retinol X receptors, hereafter referred to as (RXR), RXR belongs to the nuclear receptors, which are essential in the metabolism of cells and the whole body. However, the role of RXR in host defense against viral infection remains unknown. Nuclear receptors (NRs) represent a large family of transcription factors involved in a broad spectrum of biological events, such as development, reproduction, and metabolism. (Robinson-Rechavi et al. 2003) Many NR superfamily members have emerged as key regulators of inflammation and immune responses (Daynes and Jones, 2002; Joseph et al. 2003; Ogawa et al. 2005), which enable macrophages and dendritic cells to sense its lipid environment and shapes its immune ...

Claims

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Application Information

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IPC IPC(8): C12N5/09
Inventor 田晓丽李卫东
Owner 宁波美丽人生医药生物科技发展有限公司
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