生物
细胞生物学
人巨细胞病毒
NKG2D公司
病毒复制
好斗的
核糖核酸
病毒
病毒学
基因
遗传学
细胞毒性T细胞
泛素
体外
作者
Sirwan Salman Sleman,Huaiqing Hao,Hastyar Najmuldeen,Paywast Jamal Jalal,Nahla Muhammad Saeed,Dyary Othman,Qian Zhou
出处
期刊:Viral Immunology
[Mary Ann Liebert]
日期:2022-10-01
卷期号:35 (8): 529-544
被引量:2
标识
DOI:10.1089/vim.2022.0041
摘要
The human cytomegalovirus (HCMV) UL24 and UL43 are tegument proteins that have recently been shown to interact with each other in a yeast two-hybrid system. By their overexpression in MRC5 cells, we demonstrate that these viral proteins interact with several important host proteins, especially Dicer and trans-activation response RNA binding protein. As these hots proteins are involved in regulating the production of cellular micro-RNAs, the cytomegalovirus (CMV) proteins could interfere with their actions to favor viral replication directly or through an immune escape mechanism. Double knockout of UL24 and UL43 does not show a remarkable effect on CMV entry or replication, but it significantly downregulates the expression of CMV-encoded miR-UL59, which is thought to regulate the expression of a downstream target UL16 binding protein 1 (ULBP1). Interestingly, the double knockout increases the expression of the ULBP1 recognized by the NKG2D activating receptor of natural killer cells. This study investigates the potential role of several proteins encoded by HCMV in regulating the host cellular environment to favor escape from immunity, and it also provides some basis for the future development of RNA-targeted small molecules to control HCMV infection.
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