科研之友
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摘要
Zika virus (ZIKV) is a mosquito-borne virus that has been identified as a cause of several severe disease manifestations, including congenital microcephaly and Guillain-Barre syndrome, meningoencephalitis, and myelitis. Previous studies showed that ZIKVinfected patients exhibited elevated plasma levels of interleukin 1 beta (IL-1 beta), indicating that ZIKV may activate inflammasomes. However, the molecular basis for its viral pathogenesis remains poorly understood. In this current study, we found that ZIKV infection caused severe inflammatory pathological changes and promoted IL-1 beta production in vitro and in vivo. We here demonstrate that the maturation and secretion of IL-1 beta during ZIKV infection was mediated by NLRP3 inflammasome activation and that ZIKV nonstructural protein 5 (NS5) facilitated the assembly of the NLRP3 inflammasome complex, leading to IL-1 beta activation through interaction with NLRP3 and induction of reactive oxygen species production. Collectively, our data identify NLRP3 inflammasomederived IL-1 beta production as a critical feature of inflammation during ZIKV infection. These findings offer new insights into inflammasome-mediated diseases and may provide new therapeutic options for ZIKV-associated diseases.
- 出版日期2018-6-15
- 单位广东省实验动物监测所; 中山大学
