Carrigan D R, Kabacoff C M
Virology. 1987 Jan;156(1):185-8. doi: 10.1016/0042-6822(87)90452-1.
The ability of measles virus to induce a cell-associated state of infection in the central nervous system (CNS) plays an important role in the pathogenesis of subacute sclerosing panencephalitis (SSPE), a fatal disease of children and young adults. The mechanism by which such an infection state is established is unknown, but several hypotheses have been proposed. One of these suggests that antiviral antibodies induce the nonproductive infection state by a process termed antigenic modulation. Results presented here demonstrate that antigenic modulation is not involved in the induction of a cell-associated CNS infection in newborn hamsters by the LEC strain of SSPE derived measles virus. This follows from the finding that nonproductive, cell-associated virus can be isolated from infected CNS tissues prior to the appearance of antiviral antibodies.
麻疹病毒在中枢神经系统（CNS）中诱导细胞相关感染状态的能力在亚急性硬化性全脑炎（SSPE）的发病机制中起着重要作用，SSPE是一种发生于儿童和年轻成人的致命疾病。建立这种感染状态的机制尚不清楚，但已经提出了几种假说。其中一种假说认为，抗病毒抗体通过一种称为抗原调制的过程诱导非生产性感染状态。本文给出的结果表明，抗原调制并不参与SSPE衍生的麻疹病毒LEC株在新生仓鼠中诱导细胞相关的中枢神经系统感染。这是基于以下发现：在抗病毒抗体出现之前，就可以从受感染的中枢神经系统组织中分离出非生产性的、细胞相关的病毒。
