Introduction

Introduction

Herpes simplex virus (HSV) is a common cause of infections of the skin and mucous membranes and an uncommon cause of 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 herpesvirus 8 (the cause of Kaposi's sarcoma) and herpes zoster (the virus responsible for shingles and chicken pox). They differ in many ways, but they 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 has been 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, in new cases of genital herpes the number of HSV-1 cases now matches and even exceeds that of HSV-2.

The Disease Process

To achieve an initial infection, the following conditions must apply:

• The herpes simplex virus requires transportation in 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 HSV enters the body, the infection process typically takes place as follows:

• The virus penetrates vulnerable cells in the lower layers of skin tissue and attempts to replicate itself in the cell nuclei. Scientists are close to decoding the genetic structure of HSV and to discovering how the virus works its way into specific cells. They think that specially shaped proteins called cell adhesion molecules may facilitate the entry of HSV into healthy cells. For example, protein receptors on cells called nectin 1 and 2 may bind to some subtypes of HSV and promote the transmission of the infection from cell to cell.
• Even after it has penetrated the cells, the virus never causes symptoms in most cases.
• However, if the HSV's replication process destroys the host cells, symptoms erupt in the form of inflammation and fluid-filled blisters or ulcers. Once the fluid is absorbed, scabs form and the blisters disappear without scarring.
• After the initial replication, 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 persists in an inactive (latent) form. The virus does not replicate, 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 do recur in nearly all cases, causing a new outbreak of blisters and sores.