Congenital human cytomegalovirus infection and neurologic diseases in newborns

作     者：Xin-Yan Zhang Feng Fang Zhang Xin-Yan;Fang Feng

作者机构：Department of Pediatrics Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China 

出 版 物：《Chinese Medical Journal》 (中华医学杂志（英文版）)

年 卷 期：2019年第132卷第17期

页      面：2109-2118页

核心收录：

学科分类：1002[医学-临床医学] 10[医学] 

基　　金：This study was supported by a grant of National Natural Science Foundation of China (No. 81271807). 

主　　题：Cytomegalovirus Neurological disease Mechanism 

摘      要：Objective: This review aimed to summarize research progress regarding congenital cytomegalovirus (cCMV) infection-related nervous system diseases and their mechanisms. Data sources: All literature quoted in this review was retrieved from PubMed and Web of Science using the keywords Cytomegalovirus and Neurologic disease in English. To identify more important information, we did not set time limits. Study selection: Relevant articles were selected by carefully reading the titles and abstracts. Then, different diagnosis and clinical treatment methods for human CMV infection-related neurologic diseases were compared, and the main mechanism and pathogenesis of neurologic damage caused by CMV were summarized from the selected published articles. Results: cCMV infection is a major cause of neonatal malformation. cCMV can infect the fetal encephalon during early gestation and compromise neurodevelopment, resulting in varying degrees of neurologic damage, mainly including hearing impairment, central nervous system (CNS) infection, neurodevelopmental disorders, ophthalmic complications, cerebral neoplasms, infantile autism, epilepsy, and other neurologic abnormalities. Conclusions: cCMV infection-induced neurodevelopmental abnormalities, which were directly caused by fetal encephalon infection, thus inducing neuroimmune responses to damage nerve cells. Such abnormalities were also caused by suppression of the proliferation and differentiation of neural progenitor cells by CMV’s gene products. cCMV infection in the fetal encephalon can also inhibit neuronal migration and synapse formation and indirectly trigger placental inflammation and thus disrupt the oxygen supply to the fetus.