van Strijp J A, van Kessel K P, Miltenburg L A, Fluit A C, Verhoef J
Laboratory for Microbiology, State University of Utrecht, The Netherlands.
J Virol. 1988 Mar;62(3):847-50. doi: 10.1128/JVI.62.3.847-850.1988.
Herpes simplex virus (HSV)-infected cells can activate the human complement system without interference of specific anti-HSV antibodies. Analysis by flow cytometry showed that C3-like molecules were deposited on the membrane of the infected cell when incubated with human serum without specific antibodies. Depletion of calcium to block the classical pathway of the complement system had no effect on fluorescence intensity. The complement activation could be blocked by chelating both calcium and magnesium or by heating the serum. Furthermore, in the fluid phase C3 was converted to C3b by infected cells and not by uninfected cells. The antibody-independent activation did not lead to lysis of the virus-infected fibroblasts, indicating that the complement cascade is abrogated before formation of the membrane attack complex. This was also confirmed by measurement of the 50% hemolytic complement activities for total and alternative pathways. Polymorphonuclear leukocytes attached to infected fibroblasts after incubation of these fibroblasts with intact complement. This is most probably mediated by complement receptor binding of C3b and C3bi which is deposited on the membrane of the HSV-infected cell. Both type 1 and type 2 HSVs showed the same characteristics in complement activation and thereby mediated polymorphonuclear leukocyte adherence.
单纯疱疹病毒(HSV)感染的细胞可在无特异性抗HSV抗体干扰的情况下激活人体补体系统。流式细胞术分析表明,当与无特异性抗体的人血清孵育时,类似C3的分子沉积在感染细胞的膜上。耗尽钙以阻断补体系统的经典途径对荧光强度没有影响。螯合钙和镁或加热血清可阻断补体激活。此外,在液相中,C3由感染细胞而非未感染细胞转化为C3b。抗体非依赖性激活并未导致病毒感染的成纤维细胞裂解,表明补体级联反应在膜攻击复合物形成之前就被废除了。这也通过测量总途径和替代途径的50%溶血补体活性得到了证实。在用完整补体孵育这些成纤维细胞后,多形核白细胞附着于感染的成纤维细胞。这很可能是由沉积在HSV感染细胞膜上的C3b和C3bi的补体受体结合介导的。1型和2型HSV在补体激活方面表现出相同的特征,从而介导多形核白细胞黏附。