ZIKV infection differentially affects the transcriptional profiles in HTR8 and U251 cells.
ZIKV infection differentially affects the transcriptional profiles in HTR8 and U251 cells.
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DOI:
10.1016/j.virusres.2023.199166
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发表时间:
2023-09
期刊:
影响因子:
5
通讯作者:
Luo, Huanle
中科院分区:
文献类型:
--
作者:
Chen, Qiqi;Li, Nina;Zeng, Shike;Wu, Shu;Luo, Xin;Zhang, Shengze;Zhu, Lin;Wu, Jiani;Xie, Ting;Bai, Shaohui;Zhang, Hao;Jiang, Zhiyuan;Lin, Shaoli;Wu, Nan;Jiang, Ying;Fang, Shisong;Wang, Xin;Shu, Yuelong;Luo, Huanle
关键词:
ZIKV has a different infection pattern for placental trophoblasts and human brain cells. ZIKV infection induced interferons, inflammatory cytokines, and chemokine production. TNF-α neutralisation could promote ZIKV infection between HTR8 and U251 cells. The mechanism by which Zika virus (ZIKV) causes severe birth defects in pregnant women remains unclear. Cell tropisms in placenta and brain play a crucial role in ZIKV pathogenesis, leading to congenital Zika syndrome (CZS). To identify the host factors involved in ZIKV infection, we compared the transcriptional profiles of ZIKV-infected human first-trimester placental trophoblast cells HTR8/SVneo and a human glioblastoma astrocytoma cell line U251. Our results demonstrated that ZIKV exhibited lower rates of mRNA replication and protein expression in HTR8 than in U251 cells, while showing a higher release of infectious viral particles. However, a greater number of differentially expressed genes (DEGs) were found in ZIKV-infected U251 cells than in ZIKV-infected HTR8 cells. Several of these DEGs were enriched in distinct biological processes related to the characteristics of each cell type that may contribute to foetal damage. Both cell types exhibited activation of common interferons, inflammatory cytokines, and chemokine production upon ZIKV infection. Moreover, the neutralization of tumour necrosis factor-alpha (TNF-α) promoted ZIKV infection in both trophoblasts and glioblastoma astrocytoma cells. Overall, we identified multiple DEGs associated with ZIKV pathogenesis.
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影响因子:
4.6
作者:
Kumar A;Jovel J;Lopez-Orozco J;Limonta D;Airo AM;Hou S;Stryapunina I;Fibke C;Moore RB;Hobman TC
通讯作者:
Hobman TC
影响因子:
16.6
作者:
Caires-Júnior LC;Goulart E;Melo US;Araujo BHS;Alvizi L;Soares-Schanoski A;de Oliveira DF;Kobayashi GS;Griesi-Oliveira K;Musso CM;Amaral MS;daSilva LF;Astray RM;Suárez-Patiño SF;Ventini DC;Gomes da Silva S;Yamamoto GL;Ezquina S;Naslavsky MS;Telles-Silva KA;Weinmann K;van der Linden V;van der Linden H;de Oliveira JRM;Arrais NMR;Melo A;Figueiredo T;Santos S;Meira JGC;Passos SD;de Almeida RP;Bispo AJB;Cavalheiro EA;Kalil J;Cunha-Neto E;Nakaya H;Andreata-Santos R;de Souza Ferreira LC;Verjovski-Almeida S;Ho PL;Passos-Bueno MR;Zatz M
通讯作者:
Zatz M
影响因子:
16.6
作者:
Hirsch, Alec J.;Roberts, Victoria H. J.;Streblow, Daniel N.
通讯作者:
Streblow, Daniel N.
影响因子:
158.5
作者:
Driggers, R. W.;Ho, C. -Y.;Vapalahti, O.
通讯作者:
Vapalahti, O.
影响因子:
6
作者:
de Sousa, Jorge R.;Azevedo, Raimunda S. S.;Vasconcelos, Pedro F. C.
通讯作者:
Vasconcelos, Pedro F. C.