skip to Main Content

Learn from yesterday, live for today, hope for tomorrow. The important thing is to not stop questioning..


For those looking to understand the herpes simplex virus more in-depth, this herpes scientific information can provide a brief overview of the virus’s complexities and characteristics.

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 after the primary infection.

This means that following the initial infection the herpes virus lies dormant for periods of time. It hides within the healthy cells of the body to get protection from the antibodies produced against it by the hosts’ immune system. When inactive, the virus inhabits the cell in a 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, increased arginine in diet, excessive activity and even sunlight coupled with a weakened immune system, the virus becomes activated and travels through the nerve pathways to a site on the surface of the skin where it produces an outbreak. This site is most commonly the place where the first contact was made with the virus when it was originally contracted.

The herpes virus can inhabit a cell in a latent stage lasting for months or even years. During this inactive stage it does not reproduce or spread. Throughout this latent stage, the protein coating remains strong, the cell has not mutated, and antibodies from the immune system cannot eliminate the virus.


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 is DNA and RNA, which contain the genetic blueprint for the cell and the body. Viruses, unlike cells, genetically 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 potentially can lead to that cell dying or being engulfed by the hosts immune system.

The virus that inhabits a cell is a parasite and will drain energy from the host cell. The virus, encased in a protein coating, moves through the inter-cellular 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.

There are two main types of Herpes Simplex Viruses (HSV) which are HSV 1 and HSV 2. These constitute 2 of the at least 8 known herpes virus strains. 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. HSV 1 is responsible for more than 90% of orolabial 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.

In general genital herpes infections are caused by the herpes simplex virus type 2 (HSV2): 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 far less defined structure known as the tegument. The whole virus is contained in a membrane which is made up from proteins which 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 which the hosts immune system is able to recognize the virus. They also permit the virus to bind with the host cell membrane to enable the virus to gain entry into the host cell.

The hosts immune system will try to get rid of the invading virus by mounting an antibody response, as well as producing white blood cells which will destroy cells that have been recognized as being  infected by the virus. 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 extra-cellular viruses are neutralized whilst intra-cellular viral replication and direct cell to cell transfer is unaffected. In simple terms, virus cells that escape into the blood stream may be killed, but those which stays inside the cells are not.

When a virus is detected by the immune system, the antibodies will attach themselves to the surface proteins of the virus. This will wake up the white blood cells and enable them to destroy the viral cells which are marked with the already identifiable antibodies. 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. Whereas those with a strong and healthy immune system will employ this viral action at a more efficient level, thus preventing the amount of outbreaks and viral activity that they will experience.


This Post Has 0 Comments

Leave a Reply

*Legal Disclaimer (for your safety and ours): The HSV Blog does not claim to provide official medical advice, prevent, diagnose, treat or cure any disease. Always consult your physician in the event of possible or certain HSV symptoms for professional assistance. Any results reported may not necessarily occur in all individuals. We do everything we can to help, but we do not intend or attempt to take the place of your doctor. The HSV Blog subsequently releases all liability for information provided on this Website. By deciding to use the HSV Blog, you are also agreeing 100% with this disclaimer.
Back To Top