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Herpes viruses are extremely common and around 100 have been identified in a variety of animal species. All of the herpes viruses are members of one family, the Herpesviridae, and have certain characteristics in common, such as their ability to establish latency during primary infection.

This means that following initial infection the herpes virus lies dormant for periods of time. It hides within the cells in the body as a means of protection from the antibodies produced by the immune system.

When inactive, the virus inhabits the cell in the latent stage, during which time the virus does not replicate or travel within the body. When triggered by factors such as stress, illness, poor nutrition, excessive activity and even sunlight coupled with a weakened immune system, the virus travels around nerve pathways to the site of the outbreak.

The herpes virus can inhabit a cell in a latent stage lasting months or even years. During this inactive stage it does not reproduce or spread. Most likely, during this latent stage, the protein coating remains strong, the cell has not mutated, and antibodies from the immune system cannot eliminate the virus. A good time to attack the virus is in its active stage when it leaves the host cell and inhabits cells weakened by massive replication.

Viruses are sub-cellular organisms. When outside of a living cell, they are dormant or may even die, but when they enter a cell, they take over its metabolism to ensure its own replication.

Their most important role is to take over control of the host cell DNA and use it to make copies of its own DNA (or in some viruses like HIV the genetic material may be RNA which is slightly different).

In every reproducing cell there are DNA and RNA, which contain the genetic blueprint for the cell and the body.

Viruses genetically, unlike cells, contain either RNA or DNA but not both. Since viruses have only half the genetic material for reproduction they cannot reproduce unless they attach themselves to normal cells.

Once inside the cell they can utilize the missing genetic material and reproduce. They essentially turn the host cell into a virus production unit which may lead to that cell dying or being engulfed by the host immune system.

The virus that inhabits a cell is a parasite and will drain energy from the host cell. The virus, encased in protein coating, moves through the intercellular fluid from cell to cell and multiplies rapidly in each. Left unchallenged by a strong immune system, one virus can explode into thousands and each of these into thousands more. This is the action of the herpes virus.

Genital herpes infections are caused by the herpes simplex virus (HSV): a large (150-200nm) DNA virus which consists of approximately 152,000 base pairs of double stranded DNA, encapsulated in a layer made of protein called the capsid.

The capsid is surrounded by a less well defined structure known as the tegument. The whole virus is contained in a membrane which is made up from proteins it has scavenged from the host cell. It is studded with molecules which are the unique finger print of the virus. These so called glycoproteins are very important,:- they are the basis for the host immune system being able to recognize the virus and also enable the virus to bind with the host cell membrane to enable the virus to gain entry into the host cell.

There are two types of Herpes Simplex Viruses (HSV), HSV 1 and HSV 2. These constitute two of the at least 8 known herpes viruses. The DNA sequences of HSV 1 and HSV 2 are approximately 50% identical and their encoded proteins are even more closely related. There are no genes unique to either virus. HSV1 is responsible for more than 90% of oro-labial herpes (cold sores or fever blisters) whereas type 2 is responsible for over 90% of genital herpes infections.

Those suffering with the infection may shed the virus from the skin of the genitalia, even in the absence of symptoms. This scenario is referred to as asymptomatic viral shedding.

The host immune system will try and get rid of the invading virus by mounting an antibody response, as well as producing white cells which will destroy cells that have been recognized as being virus infected. Unfortunately those antibodies which are produced early in the course of the herpes simplex infection do not prevent recurrence of the active phase of the disease.

This probably occurs because extracellular virus is neutralized whilst intracellular viral replication and direct cell to cell transfer is unaffected. In simple terms, virus that escapes into the blood stream may be killed, but that which stays inside cells, is not.

When a virus is detected by the immune system, the antibody will attach itself to one of the surface proteins of the virus. This will wake up the white cells to enable the antibody marked virus to be destroyed. This so called cell mediated response is important in the modification of the herpes infection, as patients who suffer with a compromised cellular immune system will suffer much more severe bouts of herpes.

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