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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ptacek, Jason Sung, Phillip Arvin, Ann M. Zerboni, Leigh Sen, Nandini Rajamani, Jaya Che, Xibing |
| Description | Author Affiliation: Sen N ( Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA. nandinis@stanford.edu); |
| Abstract | Varicella-zoster virus (VZV) is a human -herpesvirus that causes varicella (chickenpox) during primary infection and zoster (shingles) upon reactivation. Like other viruses, VZV must subvert the intrinsic antiviral defenses of differentiated human cells to produce progeny virions. Accordingly, VZV inhibits the activation of the cellular transcription factors IFN regulatory factor 3 (IRF3) and signal transducers and activators of transcription 1 (STAT1), thereby downregulating antiviral factors, including IFNs. Conversely, in this study, we found that VZV triggers STAT3 phosphorylation in cells infected in vitro and in human skin xenografts in SCID mice in vivo and that STAT3 activation induces the anti-apoptotic protein survivin. Small-molecule inhibitors of STAT3 phosphorylation and survivin restrict VZV replication in vitro, and VZV infection of skin xenografts in vivo is markedly impaired by the administration of the phospho-STAT3 inhibitor S3I-201. STAT3 and survivin are required for malignant transformation caused by γ-herpesviruses, such as Kaposi's sarcoma virus. We show that STAT3 activation is also critical for VZV, a nononcogenic herpesvirus, via a survivin-dependent mechanism. Furthermore, STAT3 activation is critical for the life cycle of the virus because VZV skin infection is necessary for viral transmission and persistence in the human population. Therefore, we conclude that takeover of this major cell-signaling pathway is necessary, independent of cell transformation, for herpesvirus pathogenesis and that STAT3 activation and up-regulation of survivin is a common mechanism important for the pathogenesis of lytic as well as tumorigenic herpesviruses. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 2 |
| Volume Number | 109 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2012-01-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Herpesvirus 3, Human Physiology Inhibitor Of Apoptosis Proteins Genetics STAT3 Transcription Factor Transcriptional Activation Virus Replication Aminosalicylic Acids Pharmacology Animals Benzenesulfonates Flow Cytometry Luminescent Measurements Mice Mice, SCID Phosphorylation Reverse Transcriptase Polymerase Chain Reaction Antagonists & Inhibitors Metabolism Skin Virology Research Support, N.I.H., Extramural Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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