Paul R. (Kip) Kinchington, PhD

Paul R. (Kip) Kinchington, PhD

Contact

1016 Eye and Ear Institute
203 Lothrop Street
Pittsburgh, PA 15213

Ph: 412-647-6319

Fax: 412-647-5880

kinchingtonp@upmc.edu

My Website »

Education

  • Post Doc Uniformed Services, University of the Health Sciences
  • PhD in Microbiology/Virology, University of Leeds, England (UK)
  • BSc (Hons.) in Microbiology, University of Leeds, England (UK)

Academic Affiliation

Professor, Department of Ophthalmology

Professor, Department of Microbiology and Molecular Genetics

Member, Fox Center for Vision Restoration

Member, Clinical and Translaional Science Institute (CTSI)

Director, Molecular Biology/Bioinformatics Unit, NEI supported CORE facility

Member, Graduate Program in Microbiology and Immunology (PMI)

About Research

Dr. Kinchington’s research addresses the molecular biology of human herpesviruses that cause vision loss and blindness. Varicella zoster virus (VZV) causes chickenpox upon primary infection; and zoster (or Shingles) and debilitating, difficult-to-treat pain when the virus reactivates from latency. Despite vaccines, zoster will affect a third of the population, usually in the elderly years. A second virus is HSV-1, which causes more than 200,000 episodes of blinding stromal keratitis annually. The lab uses mice to study immune control of latency of HSV-1. The interaction with the infected cell, the neuron and the host is what drives the research, since both viruses use sensory neurons to persist.  

The lab developed two models to study VZV axon transport, neuronal latency and the chronic pain that follows Zoster. The first is a cultured human sensory neuron system with a channeled microfluidics platform that separates neuron soma and axons. It enabled the first visualization of fluorescent VZV capsids moving in axons, and was the first system in which a VZV latent state could be established that could be experimentally reactivated. This model is being used with VZV mutants to understand mechanisms involved in axonal transport, latency and reactivation. The second model mimics chronic pain that frequently follows Zoster in humans. Rats inoculated in the footpad or face with live VZV develop behaviors of pain. Recent developments are the identification of virus mutants that do not cause pain and the development of gene delivery approaches to treat VZV induced pain.

Selected Publications

Markus A, Lebenthal-Loinger I, Yang IH, Kinchington PR and Goldstein RS. 2015. An in vitro model of latency and reactivation of varicella zoster virus in human stem cell-derived neurons. PLoS Pathog. 11: e1004885.

Guedon JM, Yee MB, Zhang M, Harvey SA, Goins WF and Kinchington PR. 2015. Neuronal changes induced by Varicella Zoster Virus in a rat model of postherpetic neuralgia. Virology 482: 167-180.

Guedon JM, Zhang M, Glorioso JC, Goins WF and Kinchington PR. 2014. Relief of pain induced by varicella-zoster virus in a rat model of post-herpetic neuralgia using a herpes simplex virus vector expressing enkephalin. Gene Ther. 21: 694-702.

Stinson C, Deng M, Yee MB, Bellinger LL, Kinchington PR and Kramer PR. 2017. Sex differences underlying orofacial varicella zoster associated pain in rats. BMC Neurol. 17: 95.

Kramer PR, Stinson C, Umorin M, Deng M, Rao M, Bellinger LL, Yee MB and Kinchington PR. 2017. Lateral thalamic control of nociceptive response after whisker pad injection of varicella zoster virus. Neuroscience. 356: 207-216.

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