Herpesvirus 3, one of the eight known herpes viruses currently known to be contagious for humans is also known as chicken-pox in children and adolescents, and shingles and neuralgia (postherpetic) in adult populations. By nomenclature, it is the varicella-zoster virus, abbreviated as HHV-3 (“Varicella,” 2009). General overview of the virus includes symptoms consisting of a skin rash of blister lesions, which may cover the entire body, but tend to congregate on the face, scalp, back of legs, and trunk areas. Most individuals manifest a fever, developing just prior to the appearance of the rash. Complications include: bacterial infections of the skin, brain edema, and pneumonia. Children and adolescents present higher risk factors than adults. The virus is highly contagious when spread through coughing and sneezing, but may also be spread through direct contact and aerosolization of particles from skin lesions (Arvin and Gershon 2001 6-19).
Figure 1.1 Overview of Herpesvirus 3 on Human Face
2.0 — Human Disease and Vectors — Once considered a regular childhood disease, HHV-3 has been relegated to the less frequent category in most of the developed world through aggressive and long-term vaccinations. Primary infection results in either chickenpox or shingles, rarely mitigating into more serious symptoms. However, during the infection phase, patients are far more susceptible to pneumonia, and, in some areas of the world, encephalitis. Even when the individual pox symptoms have abated, HHV-3 remains dormant in the human nervous system, called virus latency, specifically in the trigeminal and dorsal root ganglia (Steiner, et.al. 2007). However, in 12-22% of HHV-3 cases, the latent virus reactivates later in life, producing herpes zoster or shingles. There are numerous complications from shingles; postherpetic neuralgia, zoster multiplex, myelitis, herpes ophtallmicus, or zoster sine herpete. Besides being incredibly painful, shingles has now been found to lead to strokes in certain individuals (Shinglesinfo.com; Siegel and Williams, 2008).
3.0 History of HHV-3 — the first detailed description of chicken-pox was made in the 1500s in Italy. It was mistaken for small pox in the 1600s, and not until 1767 did physician William Heberden prove that the two were different. HHV-3 waited until the early 1900s, though, to be medically described, named and differentiated. The name “chicken pox” was either given because of the blisters that appear, giving the impression of being pecked by chickens; or, because the disease is such a milder form of “pox” then it took on the “smaller — or chicken” name (Solomon 2007). Because of the nature of the symptoms, it is likely that HHV-3 is a variation of a more virulent “pox,” probably Middle Eastern or North African in origin, making its way into Europe after the Crusades where, in various forms, it was a serious pandemic. Spreading through Europe, it also landed in the New World after 1492 and, like smallpox and venereal disease, wiped out a considerable number of indigenous populations. Links to the virus historically, though, do show minor mutations over the last several decades, particularly in the areas of latency, causing concern to some researchers (Wood, 2000).
4.0 Epidemics — Because HHV-3 is so infections, there have been, and continue to be, numerous small epidemics within certain population groups. Epidemic in persons under 14 may occur at anytime during the year, but are most common in late Fall and Early Winter. Medical estimates place U.S. contagion at about 4 million per year, mostly children under 14. Rarely is the disease serious, and even rare is it fatal, with a 2008 rate of 100 deaths in the United States and 9,300 hospitalizations due to HHV-3 complications. Since 1995, though, there has been a vaccine on the market, which has caused these numbers to plummet even more (“Chickenpox- Healthier You,” 2008). Even more micro-epidemics of HHV-3 often occur in certain schools, particularly those in which students live and study on campus. Most authors agree that it is a dynamic epidemic, and that it is virtually impossible not to become infected if even near anyone with the virus. Using New York City from 1940 to 1972 as an example, though, not how the basic curve of infection remains fairly stable, with only a few spikes that are clearly within line of simple population variation (Schaffer and Kot, 1985).
Figure 4.1 — Sample data of Chicken Pox infection in New York City (Ibid).
5.0 Morphology — HHV-3 is closed related to the family of herpes simplex viruses and shares much of the genome homology. The glycoproteins so prevalent in HSV are also associated with HHV-3, but there are chemical differences that are thought to result in the issue of latency. HHV-3 virons are spherical in nature, and approximately 150-200 nm in diameter. Their lipid envelop is in icosahedral form, with DNA that is single, linear, double-stranged and 125,000 nt long. The capsid is surrounded by numerous protein structures, collectively called tegument, which play crucial roles in the replication of the virus in the infected cell, and masking the virus within latency (Reinhart, 2005).
Primary infection, as noted, is from (1) either inhaled particulates through the nose or mouth, or introduction into the eye mucus through touch. (2) Once inhaled, HHV-3 moves immediately toward the lymph notes, finding their blood rich area perfect for replication, usually 1-2 days after initial infection. Fever may rise during this time since the body knows it has been invaded, but other symptoms are usually transparent. (3) Day 4-6 are the advanced replication of the virus in the bloodstream, especially in the again, blood rich liver and spleen. Individual is usually uncomfortable, aches, headaches, fatigue, fever, and lethargy. (4) the secondary viremia moves from the organs to the skin and outward mucasoid areas; produces a rash in chickenpox, and very uncomfortable nerve pain in shingles.
6.0 Vaccine — Using strains developed in the 1970s, Merck Corporation markets a chickenpox vaccine, which received FDA approval in 1995. It is a recommended, but not required, vaccination in the United States, Canada, Australian, and other parts of the world. There is some controversy over the vaccine in that immunity induced may not be lifelong, leaving adults even more susceptible and vulnerable to more severe complications from the virus. In the United States, though, vaccine coverage approaches 90% compliance, with a notable decrease in HHV-3 cases in all walks of life. To date, the vaccine is known to protect the individual for at least 10 years, and if a recurrence does occur, it is typically quite mild. In 2007, though, the Advisory Committee on Immunization Practices (ACIP — www.cdc./gov/vaccines/rec/ACIP), recommended a booster does of the vaccine to ensure the maintenance of appropriately high levels of varicalla immunity (cdc.com’ MMWR 1996, 45). Following up for older adults, in 2006 the FDA approved Zostavax for the prevention of adult onset shingles. Zostavax is a more concentrated for of the HHV-3 vaccine, designed specifically to elicit an immune response in older adults who have waning immunity to VZV as they age (Poland 2005).
7.0 Treatment — Because HHV-3 is a virus, it is not treatable through antibiotics, and only in extreme cases is an anti-viral, typically acylovir, used. . Also because of its mild nature, therapeutic treatments to less discomfort are more appropriate. Headache, fatigue, fever and muscle aches may be treated with acetaminophen, but, because of the risk of Reve’s syndrome, no aspirin. Frequent and soothing baths help with the itching, adding ground oatmeal or other soothing bath products. Calamine lotion and OTC antihistamines may control severe itching; important because scratching increases the risk of secondary, bacterial infections and disease spread (Arvin and Gershon).
8.0 Conclusions and Further Research — HHV-3, or chickenpox in children, is a relatively mild childhood disease that appears in a significant portion of an unvaccinated population. The current vaccine seems to be effective, but critics propose that it is dangerous in the long run. Further research is needed for determination of type and strain, as well as longitudinal graphing of various populations at risk for HHV-3. In addition, dormancy issue and likelihood of shingles is an important area of future research (Orrin and Goldman, 2006). Additionally, when chickenpox becomes fatal in children, it appears that the liver becomes compromised, either with anti-inflammatory drugs or through burdening it with other toxins. Further research into this phenomenon is clearly necessary (Krasner 1999).
Arvin, a. And a. Gershon, eds. Varicella-Zoster Virus: Virology and Clinical
Management. Cambridge University Press, 2009.
Centers for Disease Control and Prevention. Varicella-Chickenpox. April 2009. Cited in:
“Chickenpox — Healthier You.” CPM Medica. 2008. Cited in:
Krasner, G. “Chickenpox: Why Do Children Die?” Coalition for Informed Choice.
1999, Cited in:
Orrin, S. And G. Goldman. The Chickenpox Vaccine: A New Epidemic of Disease and Corruption. Viritualbookworm.com, 2006.
Poland, G. “The Growing Paradigm of Preventing Disease.” Annals of Internal
Medicine. 143 no. 7 (2005): 539-41.
Schaffer, W. And M. Kott. “Nearly One Dimensional Dynamics in an Epidemic.”
Journal of Theoretical Biology. 112 no. 2 (1985): 403-27.
Shinglesinfo.com. (1999). Cited in: www.shinglesinfo.com
Siegel, M. And G. Williams. Shingles: New Hope for an Old Disease. M.Evans and Company, 2008.
Solomon, D. “Chickenpox.” History of Medicine. April 27, 2007. Cited in:
Steiner, I., et.al. “The Neurotropic Herpes Viruses.” Lancet Neurology. 6 no. 11 (2007):
Wood, M. “History of Varicella Zoster Virus.” Herpes 7 no.3 (2000): 60-65.
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