Ankel H, Westra D F, Welling-Wester S, Lebon P
Hôpital Saint-Vincent-de-Paul, Faculté de Médecine Cochin-Port-Royal, Université René-Descartes, 82 Avenue Denfert-Rochereau, Paris, 75014, France.
Virology. 1998 Nov 25;251(2):317-26. doi: 10.1006/viro.1998.9432.
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, gD is the major inducer, whereas gB, gC, gE, gG, gI, and the complex of gH and gL are poor inducers. The recombinant extramembrane fragment of gD 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 gD 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.
大多数RNA病毒诱导I型干扰素的产生是由病毒衍生的双链（ds）RNA引发的。然而，逆转录病毒和DNA病毒不合成dsRNA，它们必须依赖不同的诱导机制。对于1型人类免疫缺陷病毒（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.安克尔、M.R.卡波比安奇、C.卡斯蒂列蒂和F.迪亚赞尼（1994年）。《病毒学》205卷，第34 - 43页]。在这里我们表明，对于单纯疱疹病毒1型（HSV-1），重组糖蛋白gD是主要诱导剂，而gB、gC、gE、gG、gI以及gH和gL的复合物是较弱的诱导剂。gD的重组胞外片段足以诱导与完整病毒相当的IFN-α水平。与HIV-1一样，诱导作用被一种识别脑苷脂和硫苷脂的单克隆抗体所抑制。此外，针对趋化因子受体CCR3和CXCR4的单克隆抗体也能阻断诱导作用。我们得出结论，HSV-1通过其糖蛋白gD与产生IFN的细胞上的适当受体相互作用来诱导IFN-α。基于半乳糖基脑苷脂和趋化因子受体在HIV感染中的已知受体作用，产生IFN的细胞上的此类结构也可能参与HSV-1诱导IFN-α的过程。
