Barrett A D, Dimmock N J
J Infect Dis. 1984 Jul;150(1):98-104. doi: 10.1093/infdis/150.1.98.
Preparations of defective-interfering (DI) Semliki Forest virus (SFV) differed qualitatively in their ability to protect mice against lethal SFV-induced encephalitis. The preparations fell into three categories: (1) DI virus p13a protected the majority of mice and left them immune to subsequent challenge with 100 50% lethal doses of SFV; (2) DI virus p4 protected mice to a similar extent, but the susceptibility of all surviving mice to challenge suggested that the protection was mediated without the intervention of the adaptive immune response; and (3) DI virus p5 did not protect mice even though its interference titer was similar to that of the protective preparations. How DI viruses p4 and p13a modulate this lethal infection is not clear; the failure of p4 to stimulate protective immunity suggests that nonadaptive host responses are important, but neither p4 nor p13a altered the course of infection with a heterologous neurotropic virus. Compared with avirulent SFV infection, both DI virus-modulated infections were poorly immunogenic with regard to the humoral immune response, although a minority of mice did have high levels of neutralizing antibody. Other, unknown factors are evidently at work and remain to be elucidated.
缺陷干扰（DI）型塞姆利基森林病毒（SFV）制剂在保护小鼠免受致死性SFV诱导的脑炎方面，其能力在质量上存在差异。这些制剂分为三类：（1）DI病毒p13a保护了大多数小鼠，并使它们对随后用100个50%致死剂量的SFV攻击具有免疫力；（2）DI病毒p4对小鼠的保护程度相似，但所有存活小鼠对攻击的易感性表明，这种保护是在没有适应性免疫反应干预的情况下介导的；（3）DI病毒p5即使其干扰效价与保护性制剂相似，也不能保护小鼠。DI病毒p4和p13a如何调节这种致死性感染尚不清楚；p4未能刺激保护性免疫表明非适应性宿主反应很重要，但p4和p13a都没有改变异源嗜神经病毒的感染进程。与无毒力的SFV感染相比，尽管少数小鼠确实有高水平的中和抗体，但两种DI病毒调节的感染在体液免疫反应方面的免疫原性都很差。显然还有其他未知因素在起作用，有待阐明。
