金精三羧酸通过靶向细胞和病毒因子来抑制痘苗病毒复制的早期阶段。
Aurintricarboxylic acid inhibits the early stage of vaccinia virus replication by targeting both cellular and viral factors.
作者信息
Myskiw Chad, Deschambault Yvon, Jefferies Kristel, He Runtao, Cao Jingxin
机构信息
National Microbiology Laboratory, Canadian Science Centre for Human and Animal Health, 1015 Arlington Street, Winnipeg, Manitoba R3E 3R2, Canada.
出版信息
J Virol. 2007 Mar;81(6):3027-32. doi: 10.1128/JVI.02531-06. Epub 2006 Dec 27.
Abstract
Aurintricarboxylic acid (ATA) has been shown to inhibit the replication of viruses from several different families, including human immunodeficiency virus, vesicular stomatitis virus, and the coronavirus causing severe acute respiratory syndrome. This study characterizes the inhibitory effect of ATA on vaccinia virus replication in HeLa, Huh7, and AD293 cells. Vaccinia virus replication is significantly abrogated upon ATA treatment, which is associated with the inhibition of early viral gene transcription. This inhibitory effect may be attributed to two findings. First, ATA blocks the phosphorylation of extracellular signal-regulated kinase 1/2, an event shown to be essential for vaccinia virus replication. Second, ATA inhibits the phosphatase activity of the viral enzyme H1L, which is required to initiate viral transcription. Thus, ATA inhibits vaccinia virus replication by targeting both cellular and viral factors essential for the early stage of replication.
摘要
金精三羧酸（ATA）已被证明能抑制来自几个不同病毒家族的病毒复制，包括人类免疫缺陷病毒、水疱性口炎病毒以及导致严重急性呼吸综合征的冠状病毒。本研究描述了ATA对HeLa、Huh7和AD293细胞中痘苗病毒复制的抑制作用。ATA处理后，痘苗病毒复制显著被阻断，这与早期病毒基因转录的抑制有关。这种抑制作用可能归因于两个发现。第一，ATA阻断细胞外信号调节激酶1/2的磷酸化，这一事件已被证明对痘苗病毒复制至关重要。第二，ATA抑制病毒酶H1L的磷酸酶活性，而该酶是启动病毒转录所必需的。因此，ATA通过靶向复制早期阶段所必需的细胞和病毒因子来抑制痘苗病毒复制。
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