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风疹病毒致畸作用的分子基础。

Molecular aspects of the teratogenesis of rubella virus.

机构信息

Diagnostic Virology Group, ICMR-National Institute of Virology, 20-A, Dr. Ambedkar Road, Pune, Maharashtra, 411001, India.

出版信息

Biol Res. 2019 Aug 28;52(1):47. doi: 10.1186/s40659-019-0254-3.

Abstract

Rubella or German measles is an infection caused by rubella virus (RV). Infection of children and adults is usually characterized by a mild exanthematous febrile illness. However, RV is a major cause of birth defects and fetal death following infection in pregnant women. RV is a teratogen and is a major cause of public health concern as there are more than 100,000 cases of congenital rubella syndrome (CRS) estimated to occur every year. Several lines of evidence in the field of molecular biology of RV have provided deeper insights into the teratogenesis process. The damage to the growing fetus in infected mothers is multifactorial, arising from a combination of cellular damage, as well as its effect on the dividing cells. This review focuses on the findings in the molecular biology of RV, with special emphasis on the mitochondrial, cytoskeleton and the gene expression changes. Further, the review addresses in detail, the role of apoptosis in the teratogenesis process.

摘要

风疹或德国麻疹是由风疹病毒(RV)引起的感染。儿童和成人感染通常表现为轻度出疹性发热疾病。然而,风疹病毒是导致孕妇感染后胎儿畸形和死亡的主要原因。风疹病毒是一种致畸物,是公共卫生关注的主要原因,因为据估计每年有超过 100,000 例先天性风疹综合征(CRS)病例发生。风疹病毒分子生物学领域的几条证据为致畸过程提供了更深入的了解。受感染母亲中生长中胎儿的损伤是多因素的,源自细胞损伤以及其对分裂细胞的影响。本综述重点介绍了风疹病毒分子生物学方面的发现,特别强调了线粒体、细胞骨架和基因表达变化。此外,该综述详细讨论了细胞凋亡在致畸过程中的作用。

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