Translational medicine and varicella zoster virus: Need for disease modeling

Abstract

VZV is a ubiquitous human pathogen typically encountered early in life when primary infection causes chickenpox. During this time the virus infects ganglionic neurons at all levels of the neuraxis where the virus remains latent in host neurons. The fact that >95% of the world’s inhabitants have an immunologic response to VZV highlights the problem encountered when ascribing disease etiology to VZV reactivation. There are multiple challenges and problems to better understand pathobiology of VZV latency. There is currently no suitable disease model that mirrors the human diseases caused when virus reactivates. Without a disease model, Koch’s postulates cannot be met and ascribing a causal relationship is tenuous. Without a suitable model for all facets of VZV infection, latency and reactivation, understanding of VZV pathobiology will be difficult.

Focal points

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  Benchside

  Suitable models for all facets of VZV infection, latency and reactivation are required to better understand the mechanism of VZV pathobiology.

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  Governments

  Due to the increasing number of geriatric population at risk for severe disease caused by varicella zoster virus reactivation, there is immediate need to increase funding for research studies to find suitable models for VZV infection, latency and reactivation.