【摘要】 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 （１１４８ ±２８２ Ｖｓ ９３３５ ±２００ ， Ｐ＜ ００１） ， 血尿素氮 （ Ｂ Ｕ Ｎ） 亦明显增高 （６２２ ±１０９ｍ ｍｏｌ Ｌ Ｖｓ１１６６ ±３７７ ｍ ｍｏｌ Ｌ， Ｐ＜ ００１） ， 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型变态反应的参与更多还原

【Abstract】 An experimental study has been carried out in mice to clarify whether or not antibody-dependent enhancement of hantavirus infection would take place.18 mice were intracerebrally injected 1 LD50 Chen strain virus.After 20 days,specific antibody to hemorrhagic fever with renal syndrome virus (HFRSV) was found in serum of 17 mice.Then the antibody positive mice were divided into two groups.2%methylcellulose were intraperitoneally injected in the first group and 1 LD50 Chen strain Hantavirus injected sequentially.The second group as control were similarly injected the supernatant of BHK-21 cell culture.It was found that in the first group all animals fell ill seriously and died 3～10 days after the second injection of hantavirus,and the geometric mean titer(GMT) of specific antibody against HFRSV rose significantly(11 48±2 82 Vs 93 35±2 00,P<0 01),Blood urea nitragen (BUN) also increased markedly(6 22±1 09mmol/L Vs 11 66±3 77 mmol/L,P<0 01) as compared with basal level.The specific circulatory immune complex (CIC)became positive.There was immune complex deposition on the basemembrane of glomerular capillaries and renal tubules,and HFRSV antigen could be discovered in some parts of the kidneys.The capillaries in renal cortexes and glomeruli were congestive,and some tubules had casts.However,none of the control mice(the second group)manifested abnormalities.These data suggest that antibody-dependent enhancement of hantavirus infection may occur in mice during the second exposure to HFRSV.The kidney lesions may be due to both direct damage of the virus and immune respose especially the type Ⅲ anaphylaxis.更多还原