Zika virus restriction of host antioxidant response is mediated by intracellular NS1 and reveals its ability to upregulate Bach1 expression

被引：2

作者：

Lebeau, Gregorie ^{[1
]}

El Safadi, Daed ^{[1
]}

Hoarau, Mathilde ^{[2
]}

Meilhac, Olivier ^{[2
]}

Krejbich- Trotot, Pascale ^{[1
]}

Viranaicken, Wildriss ^{[1
,2
]}

机构：

[1] Univ la Reunion, UMR IRD 249, CNRS UMR 9192, Unite Mixte Proc Infect Milieu Insulaire Trop,Pla, F-94791 St Clotilde, Reunion, France

[2] Univ La Reunion, INSERM, UMR 1188, Diabet atherothombose Reunion Ocean Indien DeTROI, Campus Sante Univ Reunion,77 Ave Docteur Jean Mar, F-97410 St Pierre, France

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2024年 / 690卷

关键词：

Antioxidant response; Zika virus; NS1; BACH1; OXIDATIVE STRESS; TRANSMISSION; INDUCTION; DEFENSE; BRAZIL; NRF2;

D O I：

10.1016/j.bbrc.2023.149312

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Zika virus (ZIKV), has gained global attention due to its association with severe disorders, including microcephaly and congenital Zika syndrome. We investigated the role of ZIKV nonstructural protein 1 (NS1) in altering the host's antioxidant response. Using a stable cell line expressing NS1, we found that NS1 significantly reduced the expression of antioxidant-related genes, including heme oxygenase 1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), and sequestosome-1 (SQSTM1), which are regulated NRF2. Interestingly, this effect was attributed to increased expression of BACH1, a factor that competes with NRF2 for binding to certain antioxidant responsive elements (ARE). Thus, ZIKV NS1-mediated disruption of the antioxidant system is linked to BACH1 overexpression. These findings offer insights into ZIKV pathogenesis and suggest potential therapeutic strategies targeting the NRF2-BACH1 axis.

引用

页数：8

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