Poly(dA:dT) Suppresses HSV-2 Infection of Human Cervical Epithelial Cells Through RIG-I Activation.
Poly(dA:dT) Suppresses HSV-2 Infection of Human Cervical Epithelial Cells Through RIG-I Activation.
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DOI：
10.3389/fimmu.2020.598884
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发表时间：
2020
影响因子：
7.3
通讯作者：
Ho WZ
中科院分区：
文献类型：
--
作者：
Shao DD;Meng FZ;Liu Y;Xu XQ;Wang X;Hu WH;Hou W;Ho WZ
Epithelial cells of the female reproductive tract (FRT) participate in the initial innate immunity against viral infections. Poly(dA:dT) is a synthetic analog of B form double-stranded (ds) DNA which can activate the interferon (IFN) signaling pathway-mediated antiviral immunity through DNA-dependent RNA Polymerase III. Here we investigated whether poly(dA:dT) could inhibit herpes simplex virus type 2 (HSV-2) infection of human cervical epithelial cells (End1/E6E7). We demonstrated that poly(dA:dT) treatment of End1/E6E7 cells could significantly inhibit HSV-2 infection. Mechanistically, poly(dA:dT) treatment of the cells induced the expression of the intracellular IFNs and the multiple antiviral IFN-stimulated genes (ISGs), including IFN-stimulated gene 15 (ISG15), IFN-stimulated gene 56 (ISG56), 2’-5’-oligoadenylate synthetase 1 (OAS1), 2’-5’-oligoadenylate synthetase 2 (OAS2), myxovirus resistance protein A (MxA), myxovirus resistance protein B (MxB), virus inhibitory protein, endoplasmic reticulum-associated, IFN-inducible (Viperin), and guanylate binding protein 5 (GBP5). Further investigation showed that the activation of RIG-I was largely responsible for poly(dA:dT)-mediated HSV-2 inhibition and IFN/ISGs induction in the cervical epithelial cells, as RIG-I knockout abolished the poly(dA:dT) actions. These observations demonstrate the importance for design and development of AT-rich dsDNA-based intervention strategies to control HSV-2 mucosal transmission in FRT.
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影响因子：
3.7
作者：
Looker KJ;Magaret AS;May MT;Turner KM;Vickerman P;Gottlieb SL;Newman LM
通讯作者：
Newman LM
DOI：
10.1016/s1473-3099(17)30405-x
发表时间：
2017-12
期刊：
The Lancet. Infectious diseases
影响因子：
--
作者：
Looker KJ;Elmes JAR;Gottlieb SL;Schiffer JT;Vickerman P;Turner KME;Boily MC
通讯作者：
Boily MC
影响因子：
7.3
作者：
Hemann EA;Gale M Jr;Savan R
通讯作者：
Savan R
影响因子：
5.4
作者：
Chauveau, Emilie;Doceul, Virginie;Vitour, Damien
通讯作者：
Vitour, Damien
影响因子：
30.5
作者：
通讯作者：
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