In 2016, the World Health Organization declared a public health emergency regarding the Zika virus (ZIKV). For pregnant women, infection with ZIKV may result in serious birth defects including microcephaly, in which infants are born with abnormally small heads and developmental problems, causing us to take great interest in the molecular mechanisms behind ZIKV pathogenesis. We have shown that ZIKV-infected human fetal neural stem cells (fNSCs) cause inhibition of the Akt-mTOR pathway, which is crucial to brain development and autophagy regulation. We have found that two proteins in ZIKV, NS4A and NS4B, work together to suppress this pathway, leading to the cellular dysregulation of fNSCs. Consequently, we consider these proteins possible targets for anti-ZIKV therapeutic intervention.
View our paper on Zika in PubMed