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Herpes simplex - Introduction

Description

An in-depth report on the causes, diagnosis, treatment, and prevention of herpes simplex.

Alternative Names

Genital herpes; Fever blisters; Cold sores; HSV-1; HSV-2

Introduction:

Herpes simplex virus (HSV) commonly causes infections of the skin and mucous membranes. Sometimes it can cause more serious infections in other parts of the body. HSV is one of the most difficult viruses to control and has plagued mankind for thousands of years.

Herpes simplex is part of a group of other herpes viruses that include human herpes virus 8 (the cause of Kaposi's sarcoma) and herpes zoster (the virus responsible for shingles and chicken pox). There are more than 80 types of herpes viruses. They differ in many ways, but the viruses share certain characteristics, notably the word "herpes," which is derived from a Greek word meaning "to creep." This refers to the unique characteristic pattern of all herpes viruses to "creep along" local nerve pathways to the nerve clusters at the end, where they remain in an inactive state for some indeterminate time.

There are two forms of the herpes simplex virus:

  • Herpes simplex virus 1 (HSV-1)
  • Herpes simplex virus 2 (HSV-2)

These viruses are distinguished by different proteins on their surfaces. They can occur separately, or they can both infect the same individual. Until recently, the general rule was to assume that HSV-1 infections occur in the oral cavity (mouth) and are not sexually transmitted, while HSV-2 attacks the genital area and is sexually transmitted. It is now widely accepted, however, that either type can be found in either area and at other sites. In fact, HSV-1 is now responsible for up to half of all new cases of genital herpes in developed countries.

The Disease Process

For infection to occur, the following conditions must apply:

  • The herpes simplex virus passes moves through bodily fluids (saliva, semen, fluid in the female genital tract) or in fluid from herpes sores.
  • The virus must have direct access to the noninfected person through injuries in their skin or mucus surfaces (such as in the mouth or genital area).

When herpes simplex virus enters the body, the infection process typically takes place as follows:

  • The virus enters vulnerable cells in the lower layers of skin tissue and tries to reproduce in the cell nuclei.
  • Even after it has entered the cells, the virus never causes symptoms in most cases.
  • However, if the virus destroys the host cells when it multiplies, inflammation and fluid-filled blisters or ulcers appear. Once the fluid is absorbed, scabs form, and the blisters disappear without scarring.
  • After the first time they multiply, the viral particles are carried from the skin through branches of nerve cells to clusters at the nerve-cell ends (the dorsal root ganglia).
  • Here, the virus lives in an inactive (latent) form. The virus does not multiply, but both the host cells and the virus survive.
  • At unpredictable times, the virus begins multiplying again. It then goes through a period called shedding. During those times, the virus can be passed into bodily fluids and infect other people. Unfortunately, a third to half of the times shedding occurs without any symptoms at all.
  • Eventually, the symptoms return in most cases, causing a new outbreak of blisters and sores.
This close-up view of early herpes outbreak shows small, grouped blisters (vesicles) and lots of inflammation (erythema).
Herpes simplex - close-up

Resources

References

Berger JR, Houff S. Neurological complications of herpes simplex virus type 2 infection. Arch Neurol. May 2008; 65(5):596-600.

Centers for Disease Control and Prevention, Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep. 2006 Aug 4;55(RR-11):1-94.

Cernik C, Gallina K, Brodell RT. The treatment of herpes simplex infections: An evidence-based review. Arch Intern Med. 2008 Jun 9;168(11):1137-1144.

Fatahzadeh M, Schwartz RA. Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management. J Am Acad Dermatol. 2007 Nov;57(5):737-63.

Gupta R, Warren T, Wald A. Genital herpes. Lancet. 2007;370:2127-2137.

Hollier LM, Wendel GD. Third trimester antiviral prophylaxis for preventing maternal genital herpes simplex virus (HSV) recurrences and neonatal infection. Cochrane Database Syst Rev. 2008 Jan 23;(1):CD004946.

Lebrun-Vignes B, Bouzamondo A, Dupuy A, Guillaume JC, Lechat P, Chosidow O. A meta-analysis to assess the efficacy of oral antiviral treatment to prevent genital herpes outbreaks. J Am Acad Dermatol. 2007 Aug;57(2):238-46. Epub 2007 Apr 9.

Wilhelmus, K. R. Therapeutic interventions for herpes simplex virus epithelial keratitis. Cochrane Database Syst Rev. 2008 Jan 23(1): CD002898.

Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ, et al. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA. 2006 Aug 23;296(8):964-73.

  • Reviewed last on: 9/19/2008
  • Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.
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