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JVI Accepts, published online ahead of print on 27 December 2006
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J. Virol. doi:10.1128/JVI.02531-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Aurintricarboxylic acid inhibits the early stage of vaccinia virus replication by targeting both cellular and viral factors

Chad Myskiw, Yvon Deschambault, Kristel Jefferies, Runtao He, and Jingxin Cao*

National Microbiology Laboratory, Canadian Science Centre for Human and Animal Health, 1015 Arlington Street, Winnipeg, MB, Canada R3E 3R2; Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada R3T 2N2

* To whom correspondence should be addressed. Email: jingxin_cao{at}phac-aspc.gc.ca.


   Abstract

Aurintricarboxylic acid (ATA) has been shown to inhibit replication of viruses from several different families, including human immuno-deficiency virus, vesicular stomatitis virus and the coronavirus causing SARS. This study characterizes the inhibitory effect of ATA on vaccinia virus replication in HeLa, Huh7, and AD293 cells. Vaccinia replication is significantly abrogated upon ATA treatment, which is associated with inhibition of early viral gene transcription. This inhibitory effect may be attributed to two findings. First, ATA blocks phosphorylation of the extracellular signal-regulated kinase 1/2, an event shown to be essential for vaccinia replication. Secondly, ATA inhibits the phosphatase activity of the viral enzyme H1L, required to initiate viral transcription. Thus, ATA inhibits vaccinia replication by targeting both cellular and viral factors essential for the early stage of replication.







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Copyright © 2006 by the American Society for Microbiology. All rights reserved.