Shingles: To itch or not to itch?

During two weeks over the summer, the medical diagnosis of shingles came up in the game Catchphrase, on TV, and in many conversations. Ironically, within this same time period my Grandma acquired shingles. This weird series of events led me to further research this awful and painful infection.

Shingles mainly appeared in conversation when the topic of chickenpox was also being discussed. Through conversation, I learned that shingles is a virus that is caused by the same virus as chicken pox. The zoster virus, which causes both infectious diseases, stays dormant or inactive in the nervous system after one has chickenpox (Nordqvist, 2013). Later in life when the virus becomes active, it targets nerves and the skin around it (Nordqvist, 2013). Nordqvist describes herpes as an irritation of the dorsal root ganglion of a nerve that causes an eruption of vesicles along one side of the body, which follows the course of the nerve (2013).

My Grandma reported feeling a burning sensation in the affected area. Researchers have been able to identify the source of pain in postherpetic neuralgia as nerve damage (Granstedt et al., 2013), but there isn’t a lot of research on the other pain, and itching that is associated with shingles. Granstedt et al. researched the cause of the itching sensation and concluded that mice that were infected with the Pseudorabies virus (PRV) strain had synchronous and cyclical neuronal firing (2013). But, what’s even more interesting is that the excessive itching in mice was not caused merely by the PRV strain, but the viral fusion protein and it’s trafficking into the neurons (Granstedt et al., 2013)!

The “leaky” neuron already allows ions to pass by the resting sodium and potassium channels, but the PRV drills holes in the axon of the neuron, making it more “leaky” (Zandonella 2013). The holes in the axon allow the ions to move more freely. This disrupts the concentration and electrical gradients of all neurons within the same area. This causes similarly damaged neurons to fire at the same time because the freely moving ions penetrate and leave the holey neurons.

Two proteins are involved in drilling the holes into neurons. Glycoprotein B is a fusion protein that drills holes into axon walls, and Us9 acts a shuttle that sends Glycoprotein B into the axons. The proteins work similar to Butch Cassidy and the Sundance kid as they take down an axon and slowly spread the infection to others. The synchronized firing would not occur however, if the glycoprotein B was present but not in the axons. Hence, viruses that lack the gene for glycoprotein B or Us9 do not have the short circuit firing and aberrant itching (Zandonella 2013).

My Grandma’s rash still burns and hurts two months after she acquired the infection! Although she says that cold washcloths help, I wish there was something more that I could do. This discovery about the Glycoprotein B and Us9 proteins are interesting, however, I wish there was a more practical application.

Zandonella, C. (2013). Shingles symptoms may be caused by neuronal short circuit. Medical News Today, Retrieved from http://www.medicalnewstoday.com/releases/265966.php

Granstedt, A., Bosse, J., Thiberge, S., & Enquist, L. (2013). In vivo imaging of alphaherpesvirus infection reveals synchronized activity dependent on axonal sorting of viral proteins. Proceedings of the National Academy of Sciences of the United States of America, Retrieved from http://www.pnas.org/content/early/2013/08/21/1311062110.abstract

Nordqvist , C. (2013). What is shingles? what causes shingles? . Medical News Today, Retrieved from http://www.medicalnewstoday.com/articles/154912.php