Varicella virus-host interactions during latency and reactivation: lessons from simian varicella virus
- 1University of California, Irvine, United States
Varicella zoster virus (VZV) is a neurotropic alphaherpesvirus and the causative agent of varicella (chickenpox) in humans. Following primary infection, VZV establishes latency in the sensory ganglia and can reactivate to cause herpes zoster, more commonly known as shingles, which causes significant morbidity and sometimes mortality in the elderly. Because VZV infection is highly restricted to humans, the development of a reliable animal model has been challenging and our understanding of VZV pathogenesis remains incomplete. As an alternative, infection of rhesus macaques with the homologous simian varicella virus (SVV) recapitulates the hallmarks of VZV infection and thus constitutes a robust animal model to provide critical insights into VZV pathogenesis and the host antiviral response. In this model, SVV infection results in the development of varicella during primary infection, generation of an adaptive immune response, establishment of latency in the sensory ganglia and viral reactivation upon immune suppression. In this review, we discuss our current knowledge about host and viral factors involved in the establishment of SVV latency and reactivation as well as the important role played by T cells in SVV pathogenesis and antiviral immunity.
Keywords: herpesvirus, viral latency, varicella zoster virus, simian varicella virus, non-human primates, Viral reactivation, shingles
Received: 02 Oct 2018;
Accepted: 07 Dec 2018.
Edited by:Benedikt B. Kaufer, Freie Universität Berlin, Germany
Reviewed by:Donald S. Schmid, Centers for Disease Control and Prevention (CDC), United States
Stefan Oliver, Stanford University, United States
Copyright: © 2018 Sorel and Powers. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Ilhem M. Powers, University of California, Irvine, Irvine, United States, email@example.com