Paul R. (Kip) Kinchington, PhD

Dr. Kinchington’s research addresses molecular biology of human herpesviruses that cause vision loss and blindness.  Most of the lab works on Varicella zoster virus (VZV), which causes chickenpox upon primary infection, and Herpes zoster (“Shingles”) when the virus reactivates from neuronal latency.  We know little of the latent state in neurons.  Zoster is also frequently complicated by debilitating, difficult-to-treat pain through unclear mechanisms.  Despite VZV vaccines being available, zoster occurs in many as they age or become immune impaired. 

The lab studies how VZV interacts with the infected cell, particularly human neurons. We are using a cultured human neuron system derived from embryonic stem cells, often in a channeled microfluidics culture platform that separates neuron soma and axons. This model was the first to enable visualization of fluorescent VZV capsids moving in axons and was the first system in which a VZV model of the latent state could be established that could be experimentally reactivated. Cultured neurons are used with recombinant VZV mutants to understand the “round trip” process of axonal transport, latency, reactivation and returned axonal transport to the periphery: and the role of a latency-associated RNA termed VLT. A second model is to investigate exploit rats to study the chronic pain that frequently follows Zoster.  VZV in rats at the footpad or face induces mechanical hypersensitivity and pain lasting weeks.  The rat model is being used with conditional replicating recombinant VZV to identify requirements for inducing pain: and use of gene delivery approaches to treat VZV pain.