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为阐明肾综合征出血热 （ Ｈ Ｆ Ｒ Ｓ） 能否产生抗体依赖感染增强现象 （ Ａ Ｄ Ｅ） ， 我们作了小鼠实验研究。先给１８只乳鼠颅内注射１ Ｌ Ｄ５０ 陈株病毒， 使其发生不显性感染， ２０ｄ 后， 其中１７ 只小鼠血清中出现 Ｈ Ｆ Ｒ Ｓ特异性 Ｉ Ｆ Ａ 抗体。将此１７ 只小鼠分为二组， 第一组在腹腔注射２ ％ 甲基纤维素后再向腹腔注射１ Ｌ Ｄ５０ 陈株病毒； 第二组 （ 对照） 仅向腹腔注射地鼠肾细胞 （ Ｂ Ｈ Ｋ－ ２１） 培养上清液。结果第一组于第２ 次攻毒后２ ～１０ｄ 先后发病死亡， 死前血清特异性 Ｉ Ｆ抗体几何平均滴度较基础值增长７ 倍多 （１１４８ ±２８２ Ｖｓ ９３３５ ±２００ ， Ｐ＜ ００１） ， 血尿素氮 （ Ｂ Ｕ Ｎ） 亦明显增高 （６２２ ±１０９ｍ ｍｏｌ Ｌ Ｖｓ１１６６ ±３７７ ｍ ｍｏｌ Ｌ， Ｐ＜ ００１） ， 血清中查出特异性免疫复合物， 肾小球和肾小管基底膜有免疫复合物沉积， 并查到特异性抗原， 肾皮质及肾小球毛细血管充血， 部分肾小管内有管型发现， 而对照组无上述变化。这些结果提示小鼠二次感染后可发生抗体介导的感染增强现象， 而其肾脏病变除病毒之直接作用外， 尚可能有免疫反应尤其是Ⅲ型变态反应的参与
In order to elucidate whether HFRS is associated with increased ADD (A D E), we performed mouse studies. Twenty-eight infants were injected intracranially with 1 L of D50 strain of virus to induce an insignificant infection. After 20 days, 17 HspRs-specific I F A antibodies appeared in the sera of 17 mice. The 17 mice were divided into two groups. The first group was injected intraperitoneally with 1 L D50 strain of virus after intraperitoneal injection of 2% methylcellulose. The second group (control) B H K-21) Culture supernatant. Results The first group died after 2 ~ 10 days after the second challenge. The geometric mean titers of serum specific I F antibody before death increased more than 7 times (1148 ± 282 Vs 9335 ± 200, P <001), blood urea nitrogen (B U N) was also significantly higher (622 ± 109 m mol L Vs 1166 ± 377 m mol L, P <001 ), Serum specific immune complexes detected, glomerular and tubular basement membrane immune complex deposition, and found that specific antigen, renal cortex and glomerular capillary congestion, some of the tubular tubules Found, while the control group without the above changes. These results suggest that antibody-mediated enhancement of infection may occur after secondary infection in mice, and that nephropathy, in addition to the direct effects of the virus, may have an immune response, particularly type III allergy