For its extreme antiquity, the virus that causes chicken pox has a surprising sparse documented history. The earliest clear reference to the virus is actually to an emergence of its latent form as shingles, also called zoster. The ancient Greeks called it zoster after word for girdle, while shingles comes from the latin word cingulus (belt) both referring to the most common site of emergence along peripheral nerves of the back that wrap around the abdomen. There are many theories, but as far as I know, no one has successfully explained how it got the name chicken pox.
It was not until histological and immunological investigations in the early twentieth century that the relationship between the primary phase infection, chicken pox (varicella), and the emergence of the latent virus as shingles (zoster) was confirmed. Into the 18th century, chicken pox and smallpox were commonly confused as a severe and mild form of the same disease. There are subtle differences between the rashes than can distinguish them. Chicken pox produces watery pustules that concentrate on the head and trunk of the body, while smallpox lesions become hard and dimpled and are concentrated on the appendages. Chicken pox lesions are sparse or absent from the palms of the hands and soles of the feet, while these areas are often heavily covered by smallpox lesions. But, both diseases can cause lesions anywhere in the body including internal cavities and both can leave deep scars. They are also, of course, distinguished by their mortality rates. Smallpox has a mortality rate of around 30%, while chicken pox has a mortality rate of less than 1%. However, pregnant women and immune compromised patients are at high risk for life threatening complications from chicken pox. The blisters can also develop secondary bacterial infections that can become life threatening. Unlike chicken pox, smallpox requires a constant supply of non-immune hosts to persist in a community.
The lifecycle of the varicella virus is ideal to persist in small communities over many generations without outside introduction. It is primarily transmitted as a respiratory virus, but it can also be transmitted by contact with fluid from the blisters. Both routes are critical. Respiratory transmission allows it to spread rapidly while contact with blisters transmission allows it to persist in the community (more on this below).
As the virus enters the body it replicates for 10 to 21 days before the chicken pox rash of virus filled blisters appears. Meanwhile, some of the virons are infecting the peripheral nerves where the virus becomes dormant (latent). A couple days before the rash appears people feel unwell with fatigue, headache and potentially a fever, and they become contagious by coughing or sneezing. By spreading the virus before the rash appears, they spread the virus far and wide before the disease is recognized and isolated.
The blisters usually appear first on the scalp and on the trunk of the body with the number of blisters increasing with increasing age of the person. Young children can have as few as a dozen or less, while adults can have thousands of blisters. Over one to two weeks, the immune system gains the upper hand and the pustules scab over. Once the rash is scabbed over, the person is no longer contagious.
The length of time it takes for the rash to stop depends completely on the strength of the immune system. The virus can remain dormant in the peripheral nerves for 50 years or more emerging when either the peripheral nerves become inflamed (often by injury) or immune suppression develops. It reemerges as shingles (zoster), a highly painful, high density group of blisters that break out along the line of the peripheral nerve they come from, usually spinal peripheral nerves. It will looks something like a whip mark of blisters wrapping around the body from the back to the front. Fluid from these blisters can cause chicken pox in non-immune people. This is a generational persistence strategy. In small communities, the virus persists by being transmitted from an elder’s shingles to children born after the last epidemic.
Life long immunity usually follows recovery from chicken pox. Young children who only have a few lesions in their first infection can contract chicken pox a second time. It is also possible for vaccinated people to develop a usually mild case of chicken pox. In the United States vaccine acceptance is high enough that many people under age 25 have never seen a case of chicken pox. There is little doubt that if vaccination coverage wains, chicken pox will quickly become endemic again.
Origins and Evolution
The ancestral Varicella-Zoster Virus (VZV), that causes chicken pox and shingles, co-evolved with apes, hominids and humans. Along with VZV, its closest alphaherpesvirus relatives herpes simplex 1 (HSV1, ‘cold sores’) and herpes simplex 2 (HSV2, genital herpes) have a common ancestor that is approximately 120 million years old. If the age estimates for the herpes phylogenetic tree are accurate, the evolution of the alphaherpesviruses (VZV, HSV1, HSV2) coincides with the split of Africa from the supercontinent Godwanaland.
VZV has the ideal lifecycle to persist in small, isolated groups of humans, allowing it to easily survive through all three human epidemiological transitions. Latency and re-emergence in elders allowed the virus to survive in small hunter-gatherer groups, and continues to remain an advantage today. This process was observed in action on the small mid-Atlantic island of Tristan de Cunha where the population of about 200 people only experienced chicken pox outbreaks after an elder first exhibited shingles (Grose, 2012).
Phylogeny of VSV supports its origin in Africa before humans left the continent and subsequent spread through the world. Regionalism has likely occurred because VZV viruses undergo few replications per infection before they become latent so there is little chance for mutation or recombination between the clades (though it does occur). Once many more sequences are available correlations between VZV evolution and human migration should become more clear. The history of the chicken pox virus still has a long way to go. As a DNA virus, it is possible that it may be found in ancient DNA but as a virus with a low mortality rate, it will be extremely difficult to find specimens with a high enough viral copy number to detect. Those rare mummies found with pox scars should be tested for both the smallpox virus and varicella-zoster virus. Regardless we must be careful distinguishing smallpox and chicken pox in the historic record.
Grose, C. (2012). Pangaea and the Out-of-Africa Model of Varicella-Zoster Virus Evolution and Phylogeography. Journal of Virology, 86(18), 9558–9565. doi:10.1128/JVI.00357-12
Schmidt-Chanasit, J., & Sauerbrei, A. (2011). Evolution and world-wide distribution of varicella–zoster virus clades. Infection, Genetics and Evolution, 11(1), 1–10. doi:10.1016/j.meegid.2010.08.014
Wood, M. J. (2000). History of Varicella Zoster Virus. Herpes : the Journal of the IHMF, 7(3), 60–65.
Centers for Disease Control and Prevention (CDC): Chicken Pox (Varicella) Information portal. Last updated February 26, 2014.
CDC, Varicella: People at High Risk for complications. Nov. 16, 2011.
Conger, Cristen. “How Chicken Pox Works” 11 March 2008. HowStuffWorks.com. <http://health.howstuffworks.com/skin-care/problems/medical/chicken-pox.htm> 24 May 2014.