Paul R Kinchington, PhD (better known as "Kip") studies viruses that cause infections of the eye. He has been at the University of Pittsburgh since 1991, and holds faculty position in the Department of Ophthalmology. He works mostly on two herpesviruses, namely Herpes simplex virus type 1 (HSV-1), which causes potentially blinding recurrent corneal infections: and Varicella Zoster Virus (VZV) which causes chickenpox in children and Herpes Zoster ("Shingles") when it reactivates from neuronal latency, particularly in the elderly and immune compromised. He seeks to understand how these herpesviruses switch between active growth (where more virus is made) and latency, which occurs in neurons of the host and remains for life. He uses molecular biology to dissect the genes and mechanisms used to infect and damage both cells of the eye and the peripheral nervous system.
He also directs a Molecular Biology core module (and has done for more than 30 years) that has been continually funded by the National Eye Institute through a Center of Research Excellence (CORE) grant. Its mission is to help other researchers in their vision related research programs, providing services and expertise, as well as the ability to teach in such methods. These include the manipulating and preparation of DNA and RNA, the generating of recombinant viruses and /or virus based expression systems, and molecular screening methods including CRSPR-cas9 -based techniques. The Module also provides skills in basic high output transcriptome expression methods such as RNAseq.
There are three different projects that concern VZV and Shingles, which often affects the head and eye to cause blinding keratitis, ocular pain that can be very severe and corneal anesthesia. The first is address why VZV causes acute and pain and chronic pain states (often called post herpetic neuralgia, or PHN). His group worked with others to develop an exciting new facial model that mimics the pain seen in facial shingles. It is being used to not only gain mechanistic insights in pain, but also test new pain relieving treatments. The second project seeks to understand how the virus co-operates with neurons and nerve cells to stay in the latent state for life, and then why it awakens to cause Herpes zoster. His group co-developed a cultured human neuron platform to examine virus spread in neurons, transport in axons from the periphery to the neuron nucleus and what the virus makes to maintain latency. This includes a study testing ways to remove the latent virus from neurons using CRSPR-cas9. The Third project seeks to probe why the live virus used in the VZV vaccines are attenuated. Knowing the cause of virus attenuation in skin could set the basis for deriving safer and better vaccines that still give full protection against viral diseases caused by VZV