当前位置： SCI文献检索 > IMMUNITY期刊下所有文献 > The Nucleotide Sensor ZBP1 and Kinase RIPK3 Induce the Enzyme IRG1 to Promote an Antiviral Metabolic State in Neurons.

The Nucleotide Sensor ZBP1 and Kinase RIPK3 Induce the Enzyme IRG1 to Promote an Antiviral Metabolic State in Neurons.

Abstract：

:As long-lived post-mitotic cells, neurons employ unique strategies to resist pathogen infection while preserving cellular function. Here, using a murine model of Zika virus (ZIKV) infection, we identified an innate immune pathway that restricts ZIKV replication in neurons and is required for survival upon ZIKV infection of the central nervous system (CNS). We found that neuronal ZIKV infection activated the nucleotide sensor ZBP1 and the kinases RIPK1 and RIPK3, core components of virus-induced necroptotic cell death signaling. However, activation of this pathway in ZIKV-infected neurons did not induce cell death. Rather, RIPK signaling restricted viral replication by altering cellular metabolism via upregulation of the enzyme IRG1 and production of the metabolite itaconate. Itaconate inhibited the activity of succinate dehydrogenase, generating a metabolic state in neurons that suppresses replication of viral genomes. These findings demonstrate an immunometabolic mechanism of viral restriction during neuroinvasive infection.

journal_name

Immunity

journal_title

Immunity

authors

Daniels BP,Kofman SB,Smith JR,Norris GT,Snyder AG,Kolb JP,Gao X,Locasale JW,Martinez J,Gale M Jr,Loo YM,Oberst A

doi

10.1016/j.immuni.2018.11.017

subject

Has Abstract

pub_date

2019-01-15 00:00:00

pages

64-76.e4

issue

1

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(18)30525-9

journal_volume

50

pub_type

杂志文章

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