Funding outcome

The recent Zika virus (ZIKV) outbreak had a dramatic impact as it spread throughout the Americas eventually reaching the US in 2016. While infection of adults is generally limited to flu-like symptoms, the virus has been linked to Guillain-Barre syndrome. Most importantly, ZIKV can cause microcephaly and other neurological deficits in developing fetuses when mothers become infected during pregnancy. The birth defects associated with ZIKV infection are thought to require the ability of the virus to evade antiviral defenses thereby allowing it to persist in human hosts. Our recent findings suggest that the viral protein NS5 plays an important role in this process. I will investigate how interactions between NS5 and two human proteins USP15 and Trim21 affect replication of ZIKV. The findings from this project will further our understanding of how ZIKV evades the human immune system in order to persist in the developing fetus as well as reproductive tissues