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- W2958647981 abstract "The latent state of the human herpesvirus Varicella zoster virus (VZV) has remained enigmatic and controversial. While it is well substantiated that VZV persistence is established in neurons after the primary infection (varicella or chickenpox), we know little of the types of neurons harboring latent virus genomes, if all can potentially reactivate, what exactly drives the reactivation process, and the role of immunity in the control of latency. Viral gene expression during latency has been particularly difficult to resolve, although very recent advances indicate that it is more restrictive than was once thought. We do not yet understand how genes expressed in latency function in the maintenance and reactivation processes. Model systems of latency are needed to pursue these questions. This has been especially challenging for VZV because the development of in vivo models of VZV infection has proved difficult. Given that up to one third of the population will clinically reactivate VZV to develop herpes zoster (shingles) and suffer from its common long term problematic sequelae, there is still a need for both in vivo and in vitro model systems. This review will summarize the evolution of models of VZV persistence and address new insights that have arisen from the establishment of new in vitro human neuron culture systems that not only harbor a latent state, but permit experimental reactivation and renewed virus production. These models will be discussed in light of the recent data gleaned from the study of VZV latency in human cadaver ganglia." @default.
- W2958647981 created "2019-07-23" @default.
- W2958647981 creator A5018692459 @default.
- W2958647981 creator A5046119962 @default.
- W2958647981 creator A5055544265 @default.
- W2958647981 date "2019-07-24" @default.
- W2958647981 modified "2023-09-23" @default.
- W2958647981 title "Modeling Varicella Zoster Virus Persistence and Reactivation – Closer to Resolving a Perplexing Persistent State" @default.
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