Rautemaa Riina, Helander Tuula, Meri Seppo
Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki and the Helsinki University Central Hospital, Finland.
Immunology. 2002 Jul;106(3):404-11. doi: 10.1046/j.1365-2567.2002.01421.x.
Herpes simplex virus type 1 (HSV-1) infection in neurons is lifelong and generally asymptomatic. Reactivation of this latent infection results in skin blistering whereas the respective peripheral neurons are rarely affected. Why the neuronal cells are spared while the skin cells are sacrificed is not well understood. In the present study our aim was to study whether neuronal and skin cells differ in their ability to control complement attack during HSV-1 infection. Human embryonal skin (HES) cells and neuronal Paju cells were infected by HSV-1 in vitro. Both types of infected cells activated complement but were initially resistant to membrane attack complex (MAC) deposition. During the first hours of infection the expression of the endogenous complement regulators decay accelerating factor (DAF) and CD59 increased on both HES and Paju cells. By 12 hr the infected HES cells had lost their ability to control complement attack. The expression of DAF and CD59 decreased and the cells became targets for MAC attack. In contrast, complement regulator expression on the Paju cells did not decrease below the initial level and complement C5b-9 deposition was found only on 10% of the Paju cells at 12 hr. The results suggest that HSV-infected neuronal cells are better than skin cells in protecting themselves against complement attack. This may contribute to the persistence of a latent HSV-1 infection in neuronal cells for prolonged periods.
1型单纯疱疹病毒（HSV-1）在神经元中的感染是终身性的，且通常无症状。这种潜伏感染的重新激活会导致皮肤起泡，而相应的外周神经元很少受到影响。为什么神经元细胞能够幸免而皮肤细胞却受到损害，目前还不清楚。在本研究中，我们的目的是研究在HSV-1感染期间，神经元细胞和皮肤细胞在控制补体攻击的能力上是否存在差异。人胚胎皮肤（HES）细胞和神经元Paju细胞在体外被HSV-1感染。两种类型的感染细胞都激活了补体，但最初对膜攻击复合物（MAC）的沉积具有抗性。在感染的最初几个小时内，内源性补体调节因子衰变加速因子（DAF）和CD59在HES细胞和Paju细胞上的表达均增加。到12小时时，受感染的HES细胞失去了控制补体攻击的能力。DAF和CD59的表达下降，细胞成为MAC攻击的靶点。相比之下，Paju细胞上的补体调节因子表达并未降至初始水平以下，在12小时时仅在10%的Paju细胞上发现了补体C5b-9的沉积。结果表明，HSV感染的神经元细胞在保护自身免受补体攻击方面比皮肤细胞更好。这可能有助于HSV-1在神经元细胞中长期潜伏感染的持续存在。
