Barrett A D, Guest A R, Mackenzie A, Dimmock N J
J Gen Virol. 1984 Nov;65 ( Pt 11):1909-20. doi: 10.1099/0022-1317-65-11-1909.
Certain defective interfering (DI) Semliki Forest virus (SFV) preparations completely protected the majority of mice inoculated with a normally lethal dose of SFV, and the surviving mice showed no signs of disease during the period of observation. Depending upon which DI SFV preparation was used, the survivors were resistant to challenge with 100 LD50 SFV (DI SFV p13a), or were completely sensitive (DI SFV p4), the latter having evidently failed to establish a protective immunity. In this report we compared the ability of these two DI SFV preparations to inhibit multiplication of infectious virus in mice inoculated with 10 LD50 SFV. The following conclusions emerged: virus multiplication was profoundly inhibited in the majority of mice treated with either of the DI virus preparations although there was significant multiplication in most tissues, including brain. The number of mice showing evidence of reduced infectivity titres (58%) correlated well with the 60% which survived without disease in lethality experiments. Despite the presence of infectivity, no SFV antigen or histopathological lesions were detected in brain or spinal cord. The DI virus preparations p4 and p13a altered the distribution of infectivity in the mouse in different ways: during the first 2 days of the infection modulated by DI virus p4, the infectivity titres (in brain, olfactory lobes and spleen) were comparatively high, being greater than 1% of those in mice inoculated with standard virus alone. However, from day 3, titres declined precipitously and there was little infectivity in any of the tissues investigated. On the other hand, mice treated with DI SFV p13a had, over the entire duration of infection, greatly reduced though significant infectivity in brain, olfactory lobes and spleen and very little infectivity in serum. In a minority of mice (14.5%), DI virus p13a altered the distribution of infectivity between different tissues so that there was significantly decreased virus in just one or two of the four tissues investigated, suggesting that the infection was being subtly modulated by the DI virus. Interference assays failed to detect DI SFV in any tissue samples although the effects of DI virus on infection in the mouse were obvious.
某些缺陷干扰（DI）型塞姆利基森林病毒（SFV）制剂能完全保护大多数接种了正常致死剂量SFV的小鼠，且存活小鼠在观察期内无疾病迹象。根据所使用的DI SFV制剂不同，存活小鼠对100 LD50 SFV的攻击具有抗性（DI SFV p13a），或者完全敏感（DI SFV p4），后者显然未能建立保护性免疫。在本报告中，我们比较了这两种DI SFV制剂抑制接种10 LD50 SFV的小鼠中传染性病毒增殖的能力。得出以下结论：用任何一种DI病毒制剂处理的大多数小鼠中病毒增殖均受到显著抑制，尽管在包括脑在内的大多数组织中仍有明显增殖。显示感染性滴度降低迹象的小鼠数量（58%）与致死性实验中无疾病存活的60%密切相关。尽管存在感染性，但在脑或脊髓中未检测到SFV抗原或组织病理学病变。DI病毒制剂p4和p13a以不同方式改变了小鼠体内感染性的分布：在由DI病毒p4调节的感染的前2天，感染性滴度（在脑、嗅叶和脾脏中）相对较高，大于单独接种标准病毒的小鼠的1%。然而，从第3天开始，滴度急剧下降，在所研究的任何组织中几乎没有感染性。另一方面，用DI SFV p13a处理的小鼠在整个感染期间，脑、嗅叶和脾脏中的感染性虽大幅降低但仍显著，血清中感染性极低。在少数小鼠（14.5%）中，DI病毒p13a改变了不同组织之间感染性的分布，使得在所研究的四个组织中仅有一两个组织中的病毒显著减少，这表明感染正受到DI病毒的微妙调节。干扰试验未能在任何组织样本中检测到DI SFV，尽管DI病毒对小鼠感染的影响很明显。
