Herpes Simplex Mechanism

The herpes simplex virus (HSV) is a common virus that causes episodes of small, fluid-filled blisters on the mouth, lips, skin, eyes or genitals. This very contagious infection is spread through skin-to-skin or sexual contact with an individual who is infected with the virus. It can be spread through direct contact with the blister, which allows the virus to access the body or sometimes through contact with the affected area, even when no blisters are present. Genital herpes is primarily spread through sexual contact.

It is less likely that sharing towels, utensils and cutlery carries a risk of transmission because the virus dies quickly once it is outside of the body, but avoiding contact with such items is advised if a person is known to be having an outbreak of symptoms.

After initial infection, the virus lies dormant in the body and may be reactivated later, sometimes several times a year. Herpes cannot be cured, but antiviral drugs can be used to ease symptoms and help reduce the risk of infection to others.

HSV types

There are two types of HSV and these include:

• HSV-1: This form of the virus usually causes cold sores on the lips, referred to as herpes labialis and blisters on the cornea of the eye, referred to as herpes simplex keratitis. HSV-1 can also be spread to the genital area through oral sex.

• HSV-2: This is the virus that usually causes genital herpes and it is spread through both skin-to-skin contact and sexual contact. This virus is highly contagious whether sores are present or not. Recurrence is much more common with HSV-2 compared with HSV-1.

The lesion seen in herpes contains a clear fluid in which the infective viral particles are present. The body develops antibodies to the herpes simplex virus within weeks after acquiring the infection, and these antibodies can be detected on laboratory investigations. In a person who has transmitted oral HSV 1 infection, antibodies may take around 6 weeks to develop.

Pathophysiology

HSV-1 and HSV-2 typically access the body via the genital or oral mucosa and then replicate in the stratified squamous epithelium, where they are then taken up by ramifying unmyelinated sensory nerve fibers. Next, they undergo retrograde microtubule-associated transport to the neuronal cell bodies in the dorsal root ganglia (DRG) near the spinal cord, where acute infection is followed by lifelong latent infection. The virus remains in a dormant state within this collection of nerve cells. Periodically, the virus becomes reactivated and travels via anterograde microtubule-associated transport back into the stratified squamous epithelium of skin or mucosa, where replication occurs and the virus is shed into genital or oral secretions.

The cycle of infection is controlled by the immune system on several levels. On entering the body, innate and adaptive immune processes regulate the degree of replication that takes place in the mucosa. This determines how much of the virus accesses the DRG, becomes latent and then becomes reactivated. At the DRG level, latency and reactivation is subject to immune control. After the virus has been transported to the axon terminals, the level of replication is determined by adaptive immune mechanism at the interface with epithelial cells in the mucosa. This also determines whether clinical disease or asymptomatic shedding takes place.

Reactivation and recurrence can occur many times and can be triggered by various factors including fever, stress, menstruation or immune suppression. Physical trauma such as excess exposure of the lips to the sun or a dental procedure can also trigger the development of cold sores. However, in most cases, the trigger is not known.

In nearly half of individuals infected with the virus who do not have symptoms, shedding of the virus can occur more than a week before or after symptoms present. In addition, if other infections are present, the risk of transmission in the absence of overt symptoms is higher still.