Modern concepts of the mechanisms of congenital cytomegalovirus infection development

V. Vasil’ev, N. Rogozina, I. Markin
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Abstract

The review presents modern information of domestic and foreign authors about possible pathogenetic mechanisms of the virus effect on the fetus in the case of cytomegalovirus infection in pregnant women. Immunosuppressive changes, which are a feature of the physiological course of pregnancy, create favorable conditions for the development of active cytomegalovirus infection. The virus’s ability to infect a wide range of cells in vivo and trigger a set of molecular mechanisms causes changes in placental cell differentiation, which plays a key role in transplant transmission. The processes of formation of chronic placental insufficiency, which leads to hypoxia of the fetus and to delay of intrauterine development, are separately highlighted. The literary data on non-specific metabolic changes of the mother and placental activation of proinflammatory cytokines (TNF-α, IL-1β, IL2, IL-6 and IL-8), which occur in cytomegalovirus infection and are of significant importance in formation of hypoxia of the fetus have been analyzed.In addition, the role of individual cells in preventing intrauterine infection is examined, namely the deciduous macrophages with antiviral activity, the deciduous natural killers and their activated toll-like receptors. The article also discusses the genetic predisposition to the development of manifest forms of EID, including the relationship of polymorphism of TLR2 and Arg753Gln genes with an increased risk of intrauterine infection of the fetus CMV.Characteristic properties of the virus are pronounced genetic diversity, the ability to life-long persistence in various human organs and tissues (secretory glands, lymphatic cells, kidneys, etc.) and replication without cell damage, as well as suppressing cellular immunity. The article describes the issues of genotyping of virus and the relationship of some genotypes with certain organ pathology in newborns.
先天性巨细胞病毒感染发展机制的现代概念
本文综述了国内外有关孕妇巨细胞病毒感染时病毒对胎儿可能致病机制的最新研究进展。免疫抑制变化是妊娠生理过程的一个特征,为巨细胞病毒活动性感染的发展创造了有利条件。该病毒能够在体内感染多种细胞,并触发一系列分子机制,导致胎盘细胞分化发生变化,这在移植传播中起着关键作用。慢性胎盘功能不全的形成过程,导致胎儿缺氧和延迟宫内发育,分别强调。本文对巨细胞病毒感染时母体非特异性代谢变化和胎盘促炎因子(TNF-α、IL-1β、il - 2、IL-6和IL-8)激活的文献资料进行了分析,这些因子在胎儿缺氧的形成中起重要作用。此外,还研究了个体细胞在预防宫内感染中的作用,即具有抗病毒活性的乳糜巨噬细胞、乳糜自然杀伤细胞及其激活的toll样受体。本文还讨论了明显形式EID的遗传易感性,包括TLR2和Arg753Gln基因多态性与胎儿巨细胞病毒宫内感染风险增加的关系。该病毒的特点是显著的遗传多样性,能够在人体各种器官和组织(分泌腺、淋巴细胞、肾脏等)中终身存在,并在不损伤细胞的情况下进行复制,以及抑制细胞免疫。本文介绍了新生儿病毒基因分型的问题以及一些基因型与某些器官病理的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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