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Lipid raft-associated PI3K/Akt/SREBP1 signaling regulates coxsackievirus A16 (CA16) replication

文献类型： 外文期刊

作者： Wu, Zhijun 1 ; Li, Xingzhi 1 ; Guo, Dexuan 1 ; Li, Pengfei 5 ; Zhang, Yating 1 ; Zou, Dehua 1 ; Wang, Xianhe 1 ; Xu, Jiax 1 ;

作者机构： 1.HeiLongJiang BaYi Agr Univ, Coll Life Sci & Technol, Daqing 163319, Peoples R China

2.HeiLongJiang BaYi Agr Univ, Coll Anim Sci & Vet Med, Daqing 163319, Peoples R China

3.Chinese Acad Agr Sci, State Key Lab Vet Biotechnol, Harbin Vet Res Inst, Harbin 150069, Peoples R China

4.HeiLongJiang BaYi Agr Univ, Biotechnol Ctr, Daqing 163319, Peoples R China

5.Harbin Med Univ, Dept Nephrol, Affiliated Hosp 5, Daqing 163319, Peoples R China

6.HeiLongJiang BaYi Agr Univ, Coll Sci, Daqing 163319, Peoples R China

7.HeiLongJiang Acad Agr Sci, Branch Anim Husb & Vet, Qiqihar 161005, Peoples R China

关键词： Coxsackievirus A16; Lipid rafts; PI3K/Akt signaling; SREBP1; Virus replication

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

ISSN： 0378-1135

年卷期： 2021 年 252 卷

页码：

收录情况： SCI

摘要： Coxsackievirus A16 (CA16) is one of predominant Enterovirus that possesses high pathogenicity. Lipid rafts, as cholesterol - and sphingolipid - enriched membrane nanodomains, are involved into many aspects of the virus life cycle. Our previous study found that lipid rafts integrity was essential for CA16 replication, but how lipid rafts regulate CA16 replication through activating downstream signaling remains largely unknown. Thus, in this study, we revealed that lipid rafts were required for activation of PI3K/Akt signaling at early stage of CA16 infection. Treatment with wortmannin significantly reduced the expression of virus protein, indicating PI3K/Akt signaling was beneficial for early stage of virus infection. In addition, lipid rafts integrity was also indispensable for PI3K/Akt activation during the late stage of CA16 infection, which played critical functions in mediating sterol regulatory element-binding proteins 1 (SREBP1) maturation. Whereas, over-expression of SREBP1 exhibited inhibition on virus replication, suggesting that PI3K/Akt signaling and SREBP1 might positively and negatively influence virus replication in two different stages of infection, respectively. Taken together, our study demonstrates an important role of the lipid raft-associated PI3K/Akt/SREBP1 signaling in modulating CA16 replication, which will deepen our understanding mechanism of CA16 infection.

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