Regulation of maternal-fetal virus transmission in immunologically reconstituted SCID mice infected with lactate dehydrogenase-elevating virus.
Regulation of maternal-fetal virus transmission in immunologically reconstituted SCID mice infected with lactate dehydrogenase-elevating virus.
复制标题
感染乳酸脱氢酶升高病毒的免疫重建 SCID 小鼠中母胎病毒传播的调节。
DOI：
10.1089/vim.1992.5.133
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发表时间：
1992
期刊：
影响因子：
2.2
通讯作者：
Cafruny,WA
中科院分区：
文献类型：
--
作者：
Broen,JB;Bradley,DS;Powell,KM;Cafruny,WA
持续感染乳酸脱氢酶升高病毒 (LDV) 的免疫缺陷 SCID (C.B-17 scid/scid) 小鼠无法产生 IgG 抗 LDV 抗体，并且在慢性感染期间将病毒感染传播给 95% 的后代。相比之下，在分娩前 15 天或更长时间感染的正常小鼠会产生 IgG 抗 LDV 抗体，并且仅将 LDV 感染传播给 0-46% 的胎儿。 LDV 感染的经胎盘传播取决于母体感染的时间。将免疫能力过继转移给感染 LDV 的 SCID 小鼠可保护胎儿免受母体传播的病毒感染。胎儿保护与母体 IgG 抗 LDV 的存在相关，但与胎儿 IgG 抗 LDV 水平无关，并且非免疫 SCID 小鼠的病毒血症水平不影响经胎盘病毒传播。这些结果证明了母体免疫力在保护胎儿免受感染方面的重要性，并验证了该小鼠模型用于研究经胎盘病毒传播的免疫机制的用途。
Immunodeficient SCID (C.B-17 scid/scid) mice with persistent lactate dehydrogenase-elevating virus (LDV) infection failed to produce IgG anti-LDV antibodies, and during chronic infection transmitted virus infection to 95% of their offspring. In contrast, normal mice infected 15 or more days prior to giving birth produced IgG anti-LDV antibodies and transmitted LDV infection to only 0–46% of their fetuses. Transplacental transmission of LDV infection was dependent on the timing of maternal infection. Adoptive transfer of immune competence to LDV-infected SCID mice resulted in fetal protection from maternally transmitted virus infection. Fetal protection correlated with the presence of maternal IgG anti-LDV but not with fetal levels of IgG anti-LDV, and the levels of viremia in nonimmune SCID mice did not affect transplacental virus transmission. These results demonstrate the importance of maternal immunity in protecting the fetus from infection, and validate the use of this mouse model for investigation of immune mechanisms of transplacental virus transmission.