Cytomegalovirus infection in the human placenta: maternal immunity and developmentally regulated receptors on trophoblasts converge.
Cytomegalovirus infection in the human placenta: maternal immunity and developmentally regulated receptors on trophoblasts converge.
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DOI：
10.1007/978-3-540-77349-8_21
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发表时间：
2008
影响因子：
--
通讯作者：
L. Pereira;E. Maidji
中科院分区：
文献类型：
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作者：
L. Pereira;E. Maidji
在人类怀孕期间，巨细胞病毒感染子宫胎盘界面，导致不同的结果，从胎儿宫内生长受限到永久性出生缺陷，具体取决于母亲的免疫力水平和胎龄。病毒从受感染的子宫血管传播，通过在蜕膜细胞中复制而扩增，并通过免疫复合物传播到胎盘。细胞滋养层——胎盘的上皮细胞——沿着两条不同的途径分化。首先，细胞融合成覆盖绒毛膜绒毛表面的合体滋养层，将物质从母体血液输送到胎儿血液。在第二种情况下，细胞侵入子宫间质和血管，重塑脉管系统并形成锚定绒毛。 CMV 在漂浮绒毛的细胞滋养层祖细胞中启动复制，而合体滋养层则幸免。底层细胞中这种非凡的局灶感染模式取决于随着绒毛细胞滋养层开始分化，病毒颗粒受体的上调。发育调节受体的表达可以解释病毒在空间上不同的母体和胎儿区室中的复制。受感染细胞侵袭性的降低可能会损害子宫脉管系统的重塑，限制母体血流和胎儿获取营养物质，从而导致宫内生长受限。
During human pregnancy, CMV infects the uterine-placental interface with varied outcomes from fetal intrauterine growth restriction to permanent birth defects, depending on the level of maternal immunity and gestational age. Virus spreads from infected uterine blood vessels, amplifies by replicating in decidual cells, and disseminates to the placenta in immune complexes. Cytotrophoblasts–epithelial cells of the placenta–differentiate along two distinct pathways. In the first, cells fuse into syncytiotrophoblasts covering the surface of chorionic villi that transport substances from the maternal to fetal bloodstream. In the second, cells invade the uterine interstitium and blood vessels, remodel the vasculature and form anchoring villi. CMV initiates replication in cytotrophoblast progenitor cells of floating villi, whereas syncytiotrophoblasts are spared. This extraordinary pattern of focal infection in underlying cells hinges on virion receptors being upregulated as villous cytotrophoblasts begin to differentiate. Expression of developmentally regulated receptors could explain viral replication in spatially distinct maternal and fetal compartments. Reduced invasiveness of infected cells could impair remodeling of the uterine vasculature, restrict maternal blood flow and access of the fetus to nutrients causing intrauterine growth restriction.