ZIKV infection activates the IRE1-XBP1 and ATF6 pathways of unfolded protein response in neural cells.

ABSTRACT:

Background

Many viruses depend on the extensive membranous network of the endoplasmic reticulum (ER) for their translation, replication, and packaging. Certain membrane modifications of the ER can be a trigger for ER stress, as well as the accumulation of viral protein in the ER by viral infection. Then, unfolded protein response (UPR) is activated to alleviate the stress. Zika virus (ZIKV) is a mosquito-borne flavivirus and its infection causes microcephaly in newborns and serious neurological complications in adults. Here, we investigated ER stress and the regulating model of UPR in ZIKV-infected neural cells in vitro and in vivo.

Methods

Mice deficient in type I and II IFN receptors were infected with ZIKV via intraperitoneal injection and the nervous tissues of the mice

SUBMITTER: Tan Z 

PROVIDER: S-EPMC6151056 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature