English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Significance Zika virus (ZIKV) has been identified as a cause of microcephaly. However, the mechanisms by which ZIKV disrupts neurogenesis and causes microcephaly remains poorly understood. Here, we first report that ZIKV exposure causes neural progenitor cell pyroptosis, mediated by activation of caspase-1 and gasdermin D in vivo as well as in vitro, which links ZIKV to the development and progression of microcephaly. Consistent with this notion, caspase-1 deletion or treatment with caspase-1 inhibitor VX-765 reduced ZIKV-induced inflammatory responses and pyroptosis, and robustly attenuated neuropathy and brain atrophy. Taken together, our findings provide unique perspectives on ZIKV-associated neuropathogenesis and potentially clinically applicable options for its treatment.

Neural progenitor cell pyroptosis contributes to Zika virus-induced brain atrophy and represents a therapeutic target