Woodward C G, Smith H
Br J Exp Pathol. 1975 Aug;56(4):363-72.
An avirulent strain (A7) of Semliki Forest virus formed nearly as much haemagglutinating and complement fixing antigen in the brains of adult mice as a virulent (V13) strain, yet the infectivities of the brain tissues were different by about 100-fold. It appeared therefore that defective virus particles were fomed by A7 but these were not demonstrated by fluorescent antibody studies. In short-term organ cultures of adult mouse brain, A7 derived from mouse brain showed a typical interference pattern in inoculum infectivity response curves. Furthermore, when mixed suspensions of brain-grown V13 and A7 with equal infectivities were inoculated the inoculum infectivity response patterns showed significant depressions of the V13 response at higher inocula. Such interference was not detected if chick cell grown A7 and V13 were substituted for the mouse grown virus. The avirulence of A7 in adult mice and its rapid protective effect against lethal V13 infection could be due to the production of defective interfering virus particles in the brain.
塞姆利基森林病毒的无毒株（A7）在成年小鼠脑中形成的血凝和补体结合抗原量几乎与有毒株（V13）一样多，但脑组织的感染性却相差约100倍。因此，似乎A7形成了缺陷病毒颗粒，但荧光抗体研究并未证实这一点。在成年小鼠脑的短期器官培养中，源自小鼠脑的A7在接种物感染性反应曲线中显示出典型的干扰模式。此外，当接种具有相同感染性的脑内生长的V13和A7的混合悬液时，接种物感染性反应模式显示在较高接种量时V13反应有显著降低。如果用鸡细胞培养的A7和V13替代小鼠培养的病毒，则未检测到这种干扰。A7在成年小鼠中的无毒力及其对致死性V13感染的快速保护作用可能是由于在脑中产生了缺陷干扰病毒颗粒。
