Department of Molecular Microbiology, Washington University in St. Louis School of Medicine, Saint Louis, MO 63110, United States.
Department of Medicine, Washington University in St. Louis School of Medicine, Saint Louis, MO 63110, United States; Department of Molecular Microbiology, Washington University in St. Louis School of Medicine, Saint Louis, MO 63110, United States; Department of Pathology and Immunology, Washington University in St. Louis School of Medicine, Saint Louis, MO 63110, United States.
Curr Opin Virol. 2017 Dec;27:1-7. doi: 10.1016/j.coviro.2017.09.005. Epub 2017 Nov 6.
The 2015 Zika virus (ZIKV) epidemic in the Americas led to the discovery that ZIKV causes congenital abnormalities including microcephaly, intrauterine growth restriction, and eye disease that can result in blindness. Studies in animal models and human organoid cultures, together with human epidemiological studies, have shown that ZIKV crosses the placenta and subsequently replicates within fetal tissues including the developing brain. Preferential infection of neural cell precursors causes damage to the developing fetal brain. However, a majority of congenitally infected humans do not develop microcephaly or other overt congenital abnormalities, so longitudinal epidemiological studies are necessary to more completely define the long-term consequences of in utero ZIKV infection.
2015 年美洲的 Zika 病毒(ZIKV)疫情导致人们发现 ZIKV 可导致先天性异常,包括小头畸形、宫内生长受限和眼部疾病,可导致失明。动物模型和人类类器官培养研究以及人类流行病学研究表明,ZIKV 可穿过胎盘并在包括发育中大脑在内的胎儿组织内复制。神经前体细胞的优先感染导致对发育中胎儿大脑的损害。然而,大多数先天性感染的人类并不发展为小头畸形或其他明显的先天性异常,因此需要进行纵向流行病学研究以更全面地定义宫内 ZIKV 感染的长期后果。