Epstein-Barr virus lytic replication activates and is dependent upon MAPK-interacting kinase 1/2 in a cell-type dependent manner.

被引:4
作者
Adamson, Amy L. [1 ,2 ]
Jeffus, Dana [1 ]
Davis, Alexis [1 ]
Greengrove, Eva [1 ]
机构
[1] Univ North Carolina Greensboro, Dept Biol, Greensboro, NC USA
[2] Univ North Carolina Greensboro, Dept Biol, Room 201 Eberhart Bldg, Greensboro, NC 27412 USA
关键词
Epstein-barr virus; Lytic replication; mTOR; Mnk1; 2; Rapamycin; Translation; TRANSLATION INITIATION; EBV INFECTION; MTOR; EXPRESSION; EIF4E; MNK; PHOSPHORYLATION; METASTASIS; PROTEINS; BZLF1;
D O I
10.1016/j.virol.2022.05.005
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Epstein-Barr virus (EBV) is known to manipulate its cellular environment to enhance viral replication, which can lead to dysregulation of cellular machinery, setting the stage for potential future disease. Previous research showed that under rapamycin-mediated inhibition of mTORC1, EBV lytic protein production was altered in a cell-type specific manner, suggesting that EBV differentially activates or utilizes signaling pathways in B versus epithelial cells. Here we correlated activation of the mTORC1, ERK1/2, and p38 pathways in relation to EBV lytic replication and discovered that activation of MAPK-interacting kinase 1/2 (Mnk1/2) was strongly associated with EBV lytic replication. Inhibition studies revealed that Mnk1/2 activated lytic replication in epithelial cells yet acted as an inhibitor of lytic replication in B cells. The ability of lytic epithelial cells to migrate, a potentially important aspect of metastasis, was also demonstrated to be dependent upon Mnk1/2 activity.
引用
收藏
页码:72 / 85
页数:14
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