Varicella zoster virus (shingles)

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Varicella zoster virus (shingles)

Varicella zoster virus (shingles)
Written by Bianca Brown.

The Varicella zoster virus (VZV) is one of the eight herpes viruses that belong to the family Herpesviridae and the subfamily Alphaherpesvirinae.  The Alphaherpesvirinae also includes type 1 and 2 of the herpes simplex virus (HSV), the third in this sub- family is the Varicella zoster virus, more commonly known as varicella (chickenpox) and herpes zoster (shingles).

Understanding Chickenpox and shingles
The Varicella zoster virus (VZV) is one of the eight herpes viruses that belong to the family Herpesviridae and the subfamily Alphaherpesvirinae.  The Alphaherpesvirinae also includes type 1 and 2 of the herpes simplex virus (HSV), the third in this sub- family is the Varicella zoster virus, more commonly known as varicella (chickenpox) and herpes zoster (shingles).        

The Alphaherpesvirinae is primarily distinguished by its ability to reproduce at a rapid rate, faster than other herpes viridae in its family (1).  This innate ability to reproduce quickly is what has caused the spread of this Varicella zoster virus so alarming. The charterestics of this subfamily VZV is neuro topic and establishes latency in sensory neurons.  The family of Herpesviridae is built of double-stranded DNA that causes recurring infections.  After the infections life cycle begins to come to its end, the pathogenic virus will then lie dormant with-in a protected cell.  This virus never actually becomes eradicated from the body, and re-activation of this VZV results in herpes zoster.

The Vericella zoster virus is most commonly discovered in children ages ten years and younger (2).  This virus can also be found in adults suffering from auto immune deficiencies caused by cancer, the HIV virus, adults over the age of 50 years plus or in elderly people but is not limited to.  The VZV has historically infected a large number of people dating all the way back to 1767, by a man by the name of Heberden.  Heberden was the first to distinguish the difference between the two VZV now commonly known as chicken pox and shingles (3).   In 1888 von Bokay made the determination that the direct correlation between chickenpox and shingles was that chickenpox was often developed after the exposure to shingles (4).  Following this theory of relationship between the two viruses, doctor Kundratiz  created varicella-like lesions and generalized varicella in children through inoculation with vesicle fluid from patients with zoster (5).  The relationship between chicken pox and shingles was confirmed in 1952 by Weller and Stoddard who used in-virto studies to prove that both chickenpox and shingles were in fact identical viruses (6).  Today a person who has been exposed to the Varicella zoster virus has a 20% chance of acquiring shingles in his or her life time (7).

The Vericalla zoster primarily infects the conjunctiva or epitheliuma tissue composed of cells and the mucous membrane in the upper respiratory tract (8).  This is caused when a person is exposed to an inhalant of the repertory secretions related to VZV or exposure to skin lesions.  The virus then will travel up the spinal cord and to the nucleus neurons and from there it travels towards the central nerves system along the nerve fibers until it reaches the dorsal ganglion cells.  This is a cell that is located outside of the spinal cord where it enters a latent state(9).

The onset of intense pain will accrue in most people and will arrive approximately 1 to 3 days before the actual onset of skin lesions or a rash.  This pain can often be misdiagnosed and result in delay of treatment.  The most common complication associated with the Varicella zoster virus is postherpetic neuralgis (PHN).  This is what is known as the pain that can persist for up to 4 months after the recovery of the rash or skin lesions (10).  This pain is a direct cause of damaged tissue cells and the scarring of the sensory ganglia, the nerve cells located outside the brain or spinal cord that has caused damage to the nerves that conduct impulses from the area of the body that has had the rash or lesions to the brain or spinal cord (11).  Administering antiviral agents with in the first 72 hours of the identification of the VZV can reduce the PHN in most patients (12).

The structure of the Herpes simplex virus also know as (HSV) is that of an enveloped virus, meaning that the inner nuclear membrane has been modified by the presence of herpes gycoproteins.  This now compromised membrane is weakend and is no longer structurally sound allowing the virus to be transferred if there is direct contact with mucosal surfaces or secretions of an infected person.  This virus is sensitive to re-activation when exposed to acids, detergents and organic solvents much like a virus with a lipid envelope (9).  When VZV if in a second state of topical rash and or skin lesions the virus has the greatest chance of being transferred to a secondary host.  Hence the rapid rate of success for this virus.  

A more complicated form of zoster is what is known as ophthalmic zoster.  This affects on average 7% of all cases (13).  If diagnosed with ophthalmic zoster 20% to 70% of patients suffer from ocular disease (14).  This is associated with critical scaring on the lid causing retraction restrictions, paralytic ptosis (a paralyzed eye lid), resulting of drooping of the upper eye lid,  keratitis that results in cornea damage or blindness, uveitis  that is inflimation of the iris, and secondary glaucoma,  all relating to the  involvement of the nasociliary division of the ophthalmic nerve(15).

            The Ramsay Hunt syndrome is another form of a complex zoster that results in facial or auditory nerves and consists of ipsilateral facial plasy (growth developments that can grow on the side of the face),  in combination with lesions of the external ear, tympanic membrane that surrounds the bones of the middle ear, or inflammation to the anterior two thirds of the tongue.   These symptoms can result in tinnitus, vertigo, deafness, or loss of taste.  Facial nerve paralysis usually accrues in 20% of patients with zosters and is usually identifiable 3 weeks after the first onset of a rash (16).

Identifying Varicelle zoster can be difficult due to the first stages of this viris being hidden from our naked eye, but the importance to receive antiviral medications is critical.  If you suffer from suspicion of having this virus based on preliminary onset of side effects, you can seek medical attention and receive a skin scraping to determine if in fact you have contracted VZV.  A test known as Tzanck smear can be performed by scrapping the skin lesions and then staining the sample with hematoxylin-and-eosin, Giemsa, Wright’s , toluidine blue, or Papanicolaou.  This will expose the giant cells and epithelial cells containing acidophilic intranuclear inclusions(17).  Although the Tzanck smear has been tested to be effective in helping the identification of a cell abnormality, the Tzanck smear unfortunately cannot differentiate between VZV and HSV. 

Historically VZV has been treated in kids symptomatically with calamine lotion that can be applied topically and when applied directly to the blisters will dry them out reducing the spread of the VZV as well as the irritation, tepid or oatmeal baths can be taken to relieve itching, cold compresses can be applied to the infected areas to reduce inflammation and with bed rest most children return to proper health and the virus becomes latent.  In adults suffering who are immunocompromised and are generally prescribed an antiviral medication to assist in the suppression of the VZV.   Acyclovir and Vidarabine or Valtrex are some commonly perscribed antiviral medications that have been tested to decreases both the duration and the severity of the virus.  An analogue of the nucleoside guanosine, it is phosphorylated into acyclovir triphospate.  It then inhibits viral DNA polymerase by acting as a competitive inhibiter of guanosine triphospate(18).   If taken in proper dose and is accessible due to its cost of treatment both anitvirals can be an effective treatment. Long term effects on acyclovir in HIV patients have been associated with the development of acyclovir-resistance strains of VZV (168).   The OKA live Varicella vaccine received FDA approval in March 1995.  This vaccine has been shown to be 100% effective in one clinical trial and has had success in children including immunocompromised children but is still being tested on adults and the prevention of zoster shingles (19).  Some studies show that adults who receive the OKA vaccine only carry a resistance of VZV or PHN for only one year (20).

The infectious Varicella zoster virus causes a plethora of problems for the human body.  This virus can cause direct damage to the epithelium and gonglion.  The VZV can affect the body’s skin, postherpetic neuralgia (PHN), auditory nerves, ocular disease, scaring and inflammation as well as skin lesions and paralysis’.  And although previsions have been made to control the development of Varicella zoster virus the inevitable fact is that modification of this double-stranded DNA will continue and the demand of new antiviral medications will be needed and created to maintain the advantage against this herpes virus simplex 3.  

                                                Lit cited


2. Wallace Mr, Hooper DG, Pyne JM, Graves SJ, Malone JL. Varicella immunity and clinical disease in HIV-infected adults. South Med j 1994;87:74-6.

3. Gordon JE. Chickenpox: an epidemiological review.Am J Med Sci 1962;244:362-89.

4. Von Bokay J. Uber den attiologischen Zusammenhang der Varizellan mit gewissen Fallen von Herpes Zoster Wien Zlin Wochenschr 1909;22:1323-6.

5. Bruusgarrd E.The mutual relation between zoster and varicel-la. Br J Dermatol Syphilol 1932;44:1.

6. Weller TH, Stoddard MB. Intranuclear inclusion bodies in culated with varicella vesicle fluid.J Immunol 1952;68:311.

7. Seiler HE.A study of Herpes zoster particulary in its relationship to chickenpox. J Hyg (Camb) 1949;47:253.

8. Grose C. Variation on a theme by Fenner: the pathogenesis of chickenpox. Pediatris 1981;68:735-7.


10. Gilden, D. H., B. K. Kelinschmidt-DeMasters, J. J. LaGuardia, R. Mahalingam, and R. J. Cohrs. 200. Neurologic complicationsof the reactivation of varicella-zoster virus. N. Engl. J. Med. 342:635-645.

11.Cervero, F., and J.M. Laird. 1996. Mechanisms of allodynia: interactions between sencitive machanoreceptors and nociceptors. Neuroreport 7:526-528.

12. Johnson, R.W.2001.Herpes-zoster-predicting and minimizing the impact of post-herpetic neuralgia. J. Antimicrob. Chemmother. 47(Suppl. T1):1-8.

13.Weber DM, Pellecchia Ja. Varicella pneumonia: study of prevalence in adult men. Jama 1965;192:571-72.

14. Ragozzino MW, Melton LJ III, Kurland LT, Chu CP, Perry Ho. Population-based study of Herpes zoster and its sequelae. Medine (Baltimore) 1982;61:310-6.

15. Kanski JJ. Clinical Opthalmology. 2nd ed. London: Butterworth-Heinemen; 1989.p.101.

16. Mckendall RR, Klawans HL, Nervous system complications of vercilla –zoster virus in: Vinken PJ, Bruyn GW, editors. Handbook of clinical neurology; vol34.Amsterdam: Elsevier; 1978.p.161.


18. Derse D, Cheng YC, Furman PA, St Clair MH, Elion GB. Inhibition of purified human and herpes simplexvirus-induced DNA polymerases by 9-(2-hydroxy-ethoxymethyl) guanine triphosphate. J. Biol Chem 1981;256:11447-51.

19. Takahachi M. Current status and prospects of live varicella vaccine. Vaccine 1992;10:1007-14.

20. Zerboni L, Nader S, Aoki K, Arvin AM. Analysis of the persistence of humoral and cellular immunity in children and adults immunized with varicella vaccine. J Infect Dis 1998;177:1701-4.

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