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Understanding the Herpes Virus at the Cell Level

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The word “herpes” conjures up different images for different people. Some see herpes as an ugly and annoying cold sore or blister that periodically appears on or around the lips. Others see herpes as a feared sexually transmitted disease that, once you have contracted, you have to suffer with for the rest of your life. Of course both of these images do represent the term “herpes” quite accurately for many people throughout the world, but medically speaking herpes is also appropriately applied to several lesser known afflictions. These conditions include herpes inside the mouth (herpes gingivostomatitis), herpes of the throat (herpes pharyngitis), herpes of the eye (herpes keratitis), herpes of the brain (herpes encephalitis), herpes transmitted to newborn infants (neonatal herpes), chickenpox (varicella-zoster), mono (mononucleosis) and shingles (herpes-zoster). All of these conditions are caused by one of the two closely related herpes viruses known as herpes simplex virus type 1 and herpes simplex virus type 2.

To truly understand the herpes virus it is helpful to first gain some knowledge about viruses in general. Viruses are the smallest known microbes, or infectious agents, that medical science has discovered to date. Most viruses consist of a nucleic acid surrounded by a protein coat known as a capsid; this nucleic acid-protein complex is referred to as a nucleocapsid. In more complex viruses, such as the herpes virus, the nucleocapsid is surrounded by a membrane-like structure containing carbohydrates, lipids and proteins. This membrane-like structure is referred to as an envelope. Each virus contains one of two large complex chemicals that contain the viruses genetic code which serves as a blueprint for making more viruses. This complex chemical code is either RNA (ribonucleic acid) or DNA (deozyribonucleic acid).

Unlike bacteria and more complex organisms, viruses do not carry all the equipment necessary to reproduce themselves. In order to multiply, a virus must enter a living cell, remove the cells protein coat and then use its RNA or DNA to redirect the cells synthesizing mechanism to make more copies of the virus. This process of making new viruses can actually destroy or injure the living or ‘host’ cell. If enough living host cells are injured or destroyed it results in a viral illness such as influenza (the flu), viral diarrhea or genital herpes. There are hundreds of known viruses and probably thousands of others not yet discovered. Each virus has adapted to infect a particular type of cell in a specific living organism which explains why there are so many types of viruses. Because they have become so specialized some viruses can only infect certain types of cells, for instance, liver cells or muscle cells or brain cells while leaving other cells alone. Likewise, many viruses are even limited to the type of species they can infect. In general, this usually means that viruses which infect cells in one type of animal, say a dog, can not be passed on to another type of animal, say a cat. Of course as with most rules, there are exceptions and some viruses can cause similar diseases in closely related species. Another exception is that sometimes viruses can cause also cause very different illnesses in the same species.

The term “herpesvirus” refers to any member of the herpes simplex type 1 and herpes simplex type 2 virus family. The necleocapsid of a herpes virus is surrounded by an envelope with spike-like structures projecting from the surface and contains DNA. So far, scientist have identified over 115 different herpesviruses and have found more than 50 different animal species that can be infected with some type of herpes virus. Humans appear to be a natural reservoir for at least 8 different types of the herpes viruses that normally spread from human to human and generally do not cause disease in other animals.

Coming in contact with the virus, usually through sexual intercourse, is the first in a complex series of events that result in contracting genital herpes. Projecting from the outer surface of the herpes virus are protein-carbohydrate structures called glycoproteins. Glycoproteins allow the virus to attach initially to proteoglycans, which are complex chemical structures present on the surface of living cells. After attaching to the host cell, glycopoteins then interact with the cells surface structures to trigger changes in the cell membranes cytoskeletal structure. These changes allow the viral envelope to fuse with the cell plasma membrane, essentially merging to form a changed cell. When this fusion occurs, the nucleocapsid of the herpes virus enters into the cytoplasm of the host cell, attaching tiny skeleton-like structures known as microtubules and microfilaments which form an internal transportation network used to move materials within the cell. Using this structure the DNA of the herpes virus enters the nucleus of the host cell where it makes copies of the viral DNA which are released from the cell and spread to and infect other surrounding cells. This process of generating new virus particles kills the infected host cell.

If the herpes virus remained in the skins cells where initial viral attachment occurs, chances are that a healthy immune system could eventually control the infection and rid the body of the virus. The herpes virus however has found a way to hide from the immune system by hibernating in nerve cells. For unknown reasons the herpes virus does not start the replicating process in a select number of nerve cells, instead hibernating and establishing a latent infection. When the herpes virus is hybernating it is in an inactive state and can not be detected by the immune system. This inactive state is referred to as latent infection or simply latency. Latency does not cause illness but unfortunately the latent virus can reactivate and produce more virus which, in turn, causes recurrent herpes.

How reactivation occurs is unknown but it can happen for no apparent reason or be triggered by trauma, stress, or exposure to ultraviolet radiation such as too much sunlight. Whatever the trigger, after reactivation, the herpes virus is transported from the nerve cell body to the nerve endings where it is released into the skin to replicate in the skin cells. This replication may sometimes cause full blown herpes sores outbreaks, but other times may result in “shedding” the virus which causes no recognizable symptoms. However, either way, whether this reactivation is symptomatic or asyptomatic, the person is contagious during this reactivation period and it is possible to pass on the virus to a partner. For this reason, experts recommend that people with genital herpes use condoms even when there is no obvious symptoms of an active herpes breakout.

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