Department of Biology, School of Biosciences, Humanities and Exact Sciences, São Paulo State University (UNESP), São José Do Rio Preto, São Paulo, Brazil.
Cell Biology Laboratory, Institute of Health and Biological Sciences, Federal University of Alagoas, Brazil.
Antiviral Res. 2020 Jul;179:104809. doi: 10.1016/j.antiviral.2020.104809. Epub 2020 Apr 29.
The association of Zika virus infection (ZIKV) with congenital malformation and neurological sequelae brought a significant global concern. Recent studies have shown that maternal viral infection leads to inflammation in the placental tissue. In this context, the antiinflammatory protein annexin 1 (ANXA1) has a major determination of the resolution of inflammation and it has been positively associated with antiparasitic activity in infected placental explants. Although these effects have been explored to some degree, ANXA1 expression and potential properties have not yet been fully elucidated in placentas infected with ZIKV. This study was conducted to evaluate the histopathology, inflammatory process and elucidate if ANXA1 were differently expressed in placentas of ZIKV-infected mothers. Three classification groups were used in this study: Neg/Neg (mother and placenta negative for the virus), Pos/Neg (infected mother, but no virus detected in placenta) and Pos/Pos (mother and placenta infected with ZIKV). ANXA1 was expressed in syncytiotrophoblast cells of all studied groups, and its expression was decreased in Pos/Neg group, which displayed also an increase of the inflammatory response, as evinced from the recruitment of inflammatory cells, increased levels of placenta cytokines, and evidence of impaired tissue repair. The presence of ZIKV in placentas of Pos/Pos group shows structural alterations, including detachment and disorganization of the trophoblastic epithelium. In summary, our results suggest that maternal infection with ZIKV, even without direct tissue infection, leads to a placental inflammatory response probably related to the modulation of ANXA1. After placental infection, structural changes - including inflammatory cells influx - are observed leading to placental dysfunction and reduced fetal weight. Our study sheds additional light on the outcomes of ZIKV infection in trophoblast and reveals a potential involvement of ANXA1 in the placental biology.
寨卡病毒感染(ZIKV)与先天性畸形和神经后遗症的关联引起了全球的高度关注。最近的研究表明,母体病毒感染会导致胎盘组织炎症。在这种情况下,抗炎蛋白膜联蛋白 1(ANXA1)对炎症的消退有重要决定作用,并且它与感染胎盘外植体中的抗寄生虫活性呈正相关。尽管这些作用在一定程度上得到了探索,但 ZIKV 感染胎盘中 ANXA1 的表达及其潜在特性尚未得到充分阐明。本研究旨在评估组织病理学、炎症过程,并阐明 ZIKV 感染母亲的胎盘中 ANXA1 是否有不同的表达。本研究使用了三个分类组:Neg/Neg(母亲和胎盘均未感染病毒)、Pos/Neg(感染母亲,但胎盘未检测到病毒)和 Pos/Pos(母亲和胎盘均感染 ZIKV)。ANXA1 在所有研究组的合体滋养层细胞中均有表达,而在 Pos/Neg 组中其表达减少,该组还显示出炎症反应增加,表现为炎症细胞募集增加、胎盘细胞因子水平升高以及组织修复受损的证据。Pos/Pos 组胎盘中 ZIKV 的存在显示出结构改变,包括滋养层上皮的脱落和组织紊乱。综上所述,我们的研究结果表明,母体感染 ZIKV,即使没有直接的组织感染,也会导致胎盘炎症反应,这可能与 ANXA1 的调节有关。胎盘感染后,会观察到结构变化,包括炎症细胞浸润,导致胎盘功能障碍和胎儿体重减轻。本研究进一步揭示了 ZIKV 在滋养层中的感染结局,并揭示了 ANXA1 可能参与胎盘生物学。