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World J Virol. Nov 12, 2016; 5(4): 144-154
Published online Nov 12, 2016. doi: 10.5501/wjv.v5.i4.144
Regulation of Wnt/β-catenin signaling by herpesviruses
Kevin J Zwezdaryk, Joseph A Combs, Cindy A Morris, Deborah E Sullivan
Kevin J Zwezdaryk, Joseph A Combs, Cindy A Morris, Deborah E Sullivan, Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, LA 70112, United States
Author contributions: Zwezdaryk KJ and Combs JA wrote the article, prepared the figures and tables; Morris CA and Sullivan DE outlined and edited the article.
Conflict-of-interest statement: The authors have no conflicts to disclose.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Deborah E Sullivan, PhD, Associate Professor, Department of Microbiology and Immunology, Tulane University School of Medicine, 1430 Tulane Avenue, Mail Code 8638, New Orleans, LA 70112, United States. dsulliva@tulane.edu
Telephone: +1-504-9886690 Fax: +1-504-9885144
Received: May 29, 2016
Peer-review started: May 30, 2016
First decision: July 6, 2016
Revised: July 19, 2016
Accepted: August 6, 2016
Article in press: August 8, 2016
Published online: November 12, 2016
Abstract

The Wnt/β-catenin signaling pathway is instrumental in successful differentiation and proliferation of mammalian cells. It is therefore not surprising that the herpesvirus family has developed mechanisms to interact with and manipulate this pathway. Successful coexistence with the host requires that herpesviruses establish a lifelong infection that includes periods of latency and reactivation or persistence. Many herpesviruses establish latency in progenitor cells and viral reactivation is linked to host-cell proliferation and differentiation status. Importantly, Wnt/β-catenin is tightly connected to stem/progenitor cell maintenance and differentiation. Numerous studies have linked Wnt/β-catenin signaling to a variety of cancers, emphasizing the importance of Wnt/β-catenin pathways in development, tissue homeostasis and disease. This review details how the alpha-, beta-, and gammaherpesviruses interact and manipulate the Wnt/β-catenin pathway to promote a virus-centric agenda.

Keywords: Herpesvirus, Herpes simplex virus-1, Varicella zoster virus, Cytomegalovirus, Epstein-Barr virus, Kaposi’s sarcoma-associated herpesvirus, Wnt/β-catenin, Glycogen synthase kinase-3, Axin

Core tip: The Wnt/β-catenin signaling pathway is essential for many host cell functions. Herpesviruses have evolved to manipulate and control this vital pathway to promote viral propagation, evade host immune recognition and maintain latency.