Induction of interferon-α by glycoprotein D of herpes simplex virus:: A possible role of chemokine receptors
Induction of interferon-α by glycoprotein D of herpes simplex virus:: A possible role of chemokine receptors
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DOI：
10.1006/viro.1998.9432
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发表时间：
1998-11-25
期刊：
影响因子：
3.7
通讯作者：
Lebon, P
中科院分区：
文献类型：
--
作者：
Ankel, H;Westra, DF;Lebon, P
大多数RNA病毒对I型干扰素的诱导是由病毒衍生的双链（ds）RNA启动的。然而，不合成dsRNA的逆转录病毒和DNA病毒必须依赖于不同的诱导机制。对于人类免疫缺陷病毒1型（HIV-1），重组糖蛋白120或160足以在血液来源的淋巴细胞中诱导干扰素（IFN）-α [H. Ankel，M. R.卡波比安奇角Castilletti和F. Dianzani（1994年）。Virology 205，34-43]。在这里，我们表明，对于单纯疱疹病毒1型（HSV-1）重组糖蛋白，去是主要的诱导剂，而gB，gC，gE，gG，gl，和gH和gL的复合物是不良的诱导剂。重组膜外片段足以诱导IFN-α水平与完整病毒相当。与HIV-1一样，诱导被识别β-内酰胺酶和硫苷脂的单克隆抗体抑制。此外，对趋化因子受体CCR 3和CXCR 4特异性的单克隆抗体也阻断诱导。我们得出结论，HSV-1诱导IFN-α的相互作用，其糖蛋白去与适当的受体上的IFN-产生细胞。基于半乳糖苷和趋化因子受体在HIV感染中的已知受体作用，IFN产生细胞上的这种结构也可以参与HSV-1对IFN-α的诱导。(C)北京：科学出版社.
The induction of type I interferons by most RNA viruses is initiated by virus-derived double-stranded (ds)RNA. However, retro- and DNA-viruses, which do not synthesize dsRNA, must rely on different mechanisms of induction. For human immunodeficiency virus type 1 (HIV-1), recombinant glycoproteins 120 or 160 suffice to induce interferon (IFN)-alpha in blood-derived lymphocytes [H. Ankel, M. R. Capobianchi, C. Castilletti, and F. Dianzani (1994). Virology 205, 34-43]. Here we show that for herpes simplex virus type 1 (HSV-1) recombinant glycoprotein, go is the major inducer, whereas gB, gC, gE, gG, gl, and the complex of gH and gL are poor inducers. The recombinant extramembrane fragment of go was sufficient to induce IFN-alpha levels comparable to that of intact virus. Like with HIV-1, induction was inhibited by a monoclonal antibody that recognizes cerebrosides and sulfatides. Furthermore, monoclonal antibodies specific for the chemokine receptors CCR3 and CXCR4 also blocked induction. We conclude that HSV-1 induces IFN-alpha by interaction of its glycoprotein go with appropriate receptors on IFN-producing cells. Based on the known receptor roles of galactosyl cerebrosides and chemokine receptors in HIV infection, such structures on IFN-producing cells could also participate in the induction of IFN-alpha by HSV-1. (C) 1998 Academic Press.