Reveals molecular mechanisms by which the Zika virus affects fetal brain development.

Recently, Luo Minhua of the Wuhan Institute of VirusEs of the Chinese Academy of Sciences made new progress in the study of neuro-injury mechanisms caused by the Zika virus (ZIKV), and found that the Zika virus infection of neural stem cells significantly reduced its important marker of molecular doublegein (doublecortin, DCX), for Zika virus infection affects the cerebral cortex structure and brain nerve development proposed a new potential mechanism.
work published online by Frontiers in Micorbiology.
Zika virus (ZIKA virus, ZIKV), a genus of the yellow virus in the jaundice virus, is transmitted by the Aedes aegypti mosquito and was first isolated in 1947 in monkeys in Uganda's Zika forest, hence its name.
nearly two years ago, the Zika virus has spread to Central and South America and Southeast Asia, leading to a significant increase in microcephaly and other birth defects in the region, causing global attention.
has been reported that human neural stem cells (NPC) can be infected with the Zika virus, suggesting that microcephaly may have been caused by affecting the fate of cells in neural stem cells, whose molecular mechanisms have not yet been resolved.
the study, through proteomic analysis of the human progenitor NPC for Zika virus infection, found that protein levels in cells affectthet elemental molecules of neuroprogenic cell proliferation, differentiation, and migration have changed.
and double-skin quality (DCX) plays an important role in NPC differentiation and migration.
results show that when The Zika virus infects NPC, it lowers both the protein level and the mRNA level of DCX.
, in the Zika virus-infected fetal brain model, DCX protein levels were also significantly reduced, accompanied by abnormalities in fetal weight, fetal brain weight and fetal brain size, and damage to the cerebral cortex structure.
found a correlation between NS4A and NS5 and a reduction in DCX protein levels and mRNA levels by further screening of Zika virus proteins and their expression in NPC.
these data suggest that the Regulation of The Zika virus occurs after infection, while the viral protein NS4A, NS5 is involved in the regulation of DCX.
the study revealed a link between the Zika virus and the fate of NPC cells and abnormal fetal brain development, and pointed to the important role of key molecule DCX in the pathological outcomes of cortisco infection.
, screening the viral protein NS4A, NS5 downgraded the key molecule DCX, further revealing the molecular mechanisms of the Zika virus that affect fetal brain development.
will continue to confirm that viral proteins interact with DCX.
, Jiang Feng, a postdoctoral fellow in the neurovirus discipline group of Wuhan Virus Institute, is the first author, Luo Minhua and Tang Yaping, professor of Guangzhou Women's and Children's Medical Center, are co-authors, and the work has been supported by the National Natural Science Foundation of China, the National Key Laboratory and The Guangzhou Women's and Children's Medical Center.
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